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Background. Arsenic is a toxic metalloid widely present in nature, and arsenic poisoning in drinking water is a serious global public problem. Glutathione is an important reducing agent that inhibits arsenic-induced oxidative stress and participates in arsenic methylation metabolism. Therefore, glutathione plays an important role in regulating arsenic toxicity. In recent years, a large number of studies have shown that arsenic can regulate glutathione synthesis in many ways, but there are many contradictions in the research results. At present, the mechanism of the effect of arsenic on glutathione synthesis has not been elucidated. Objective. We will conduct a meta-analysis to illustrate the effects of arsenic on GSH synthesis precursors Glu, Cys, Gly, and rate-limiting enzyme γ-GCS in mammalian models, as well as the regulation of p38/Nrf2 of γ-GCS subunit GCLC, and further explore the molecular mechanism of arsenic affecting glutathione synthesis. Results. This meta-analysis included 30 studies in vivo and 58 studies in vitro, among which in vivo studies showed that arsenic exposure could reduce the contents of GSH (SMD=−2.86, 95% CI (-4.45, -1.27)), Glu (SMD=−1.11, 95% CI (-2.20,-0.02)), and Cys (SMD=−1.48, 95% CI (-2.63, -0.33)), with no statistically significant difference in p38/Nrf2, GCLC, and GCLM. In vitro studies showed that arsenic exposure increased intracellular GSH content (SMD=1.87, 95% CI (0.18, 3.56)) and promoted the expression of p-p38 (SMD=4.19, 95% CI (2.34, 6.05)), Nrf2 (SMD=4.60, 95% CI (2.34, 6.86)), and GCLC (SMD=1.32, 95% CI (0.23, 2.41)); the p38 inhibitor inhibited the expression of Nrf2 (SMD=−1.27, 95% CI (-2.46, -0.09)) and GCLC (SMD=−5.37, 95% CI (-5.37, -2.20)); siNrf2 inhibited the expression of GCLC, and BSO inhibited the synthesis of GSH. There is a dose-dependent relationship between the effects of exposure on GSH in vitro. Conclusions. These indicate the difference between in vivo and in vitro studies of the effect of arsenic on glutathione synthesis. In vivo studies have shown that arsenic exposure can reduce glutamate and cysteine levels and inhibit glutathione synthesis, while in vitro studies have shown that chronic low-dose arsenic exposure can activate the p38/Nrf2 pathway, upregulate GCLC expression, and promote glutathione synthesis.
Shanshan Ran; Jiaqing Liu; Shugang Li. A Systematic Review of the Various Effect of Arsenic on Glutathione Synthesis In Vitro and In Vivo. BioMed Research International 2020, 2020, 1 -22.
AMA StyleShanshan Ran, Jiaqing Liu, Shugang Li. A Systematic Review of the Various Effect of Arsenic on Glutathione Synthesis In Vitro and In Vivo. BioMed Research International. 2020; 2020 ():1-22.
Chicago/Turabian StyleShanshan Ran; Jiaqing Liu; Shugang Li. 2020. "A Systematic Review of the Various Effect of Arsenic on Glutathione Synthesis In Vitro and In Vivo." BioMed Research International 2020, no. : 1-22.
The purpose of our study was to investigate the role of hypoxia-inducible factor-1α (HIF-1α) in arsenic-induced carcinogenesis. We included 39 articles for meta-analysis. The results showed that low-dose exposure to arsenic (≤ 10 μmol/L) could promote the expression of phosphatidylinositol 3-kinase (PI3K) and phosphorylation-protein kinase B (p-AKT). High-dose arsenic exposure (> 10 μmol/L) promoted the expression of PI3K, HIF-1α, vascular endothelial growth factor (VEGF), and p38MAPK (P38). Acute arsenic exposure (< 24 h) promoted the expression of PI3K, HIF-1α, and VEGF. Chronic arsenic exposure (≥ 24 h) promoted the expression of PI3K, p-AKT, and P38. Moreover, for normal tissue-derived cells, arsenic could induce the increased expression of PI3K, p-AKT, HIF-1α, and VEGF. For tumor tissue-derived cells, arsenic could induce the expression of PI3K, p-AKT, and P38. We found that arsenic exposure could activate the PI3K/AKT pathway, further induce the high expression of HIF-1α, and then upregulate the levels of miRNA-21 and VEGF, promote the expression of proliferating cell nuclear antigen (PCNA), and ultimately lead to malignant cell proliferation. Our findings indicated that arsenic could increase the expression of HIF-1α by activating the PI3K/AKT pathway and eventually induce malignant cell proliferation.
Jiaqing Liu; Qiang Niu; Yunhua Hu; Shanshan Ran; Shugang Li. The Mechanism of Trivalent Inorganic Arsenic on HIF-1α: a Systematic Review and Meta-analysis. Biological Trace Element Research 2020, 198, 449 -463.
AMA StyleJiaqing Liu, Qiang Niu, Yunhua Hu, Shanshan Ran, Shugang Li. The Mechanism of Trivalent Inorganic Arsenic on HIF-1α: a Systematic Review and Meta-analysis. Biological Trace Element Research. 2020; 198 (2):449-463.
Chicago/Turabian StyleJiaqing Liu; Qiang Niu; Yunhua Hu; Shanshan Ran; Shugang Li. 2020. "The Mechanism of Trivalent Inorganic Arsenic on HIF-1α: a Systematic Review and Meta-analysis." Biological Trace Element Research 198, no. 2: 449-463.
Objective. This study is aimed at evaluating the diagnostic value of blood lipid indicators (BLIs) for insulin resistance (IR) among major ethnic groups in Xinjiang, China, to identify the most valuable indicators and appropriate cut-off points for each ethnic group and to lay the foundation for the early detection, diagnosis, and treatment of metabolic diseases in remote rural areas. Methods. Overall, 418 Uygurs, 331 Kazakhs, and 220 Hans were randomly included in our study. The homeostasis model assessment was the gold standard for identifying IR. The receiver operating characteristic (ROC) curve was used to evaluate the diagnostic value, and the nomogram was utilized to analyze the predictive value. The size of the area under the curve (AUC) reflected the accuracy of screening and prediction. Results. Differences in races were observed in terms of IR and BLIs, and the Kazakhs had the highest IR level at 5.27 mmol/L. The correlation between IR and BLIs differed among the three races. For the Kazakhs and Hans, all BLIs, except total cholesterol (TC), were correlated to IR. However, for the Uygurs, only the triglyceride (TG) level, TG/high-density lipoprotein cholesterol (HDL-C) ratio, and TC/HDL-C ratio were associated with IR. After further adjustment of confounding factors, these indicators were still correlated to IR. BLIs that independently correlated to IR in the three nationalities had a certain diagnostic value for IR. In terms of the AUC size, the TG level was the highest in Uygurs, the TG/HDL-C ratio was the highest for Kazakhs and Hans, and the corresponding best cut-off points for IR were 1.515, 1.230, and 1.495 mmol/L, respectively. In addition, for each race, when the indicators with a certain diagnostic value were combined, the diagnostic value for IR was higher. Conclusion. BLIs had a certain diagnostic value for IR and could be used as a screening tool for IR among Uygurs, Kazakhs, and Hans in Xinjiang. These findings are extremely important for the prevention and treatment of IR and metabolic diseases in remote rural areas.
Yi-Zhong Yan; Jia-Ning Fan; Jia-Ming Liu; Yun-Hua Hu; Jiao-Long Ma; Jia He; Heng Guo; Xianghui Zhang; Xin-Ping Wang; Shu-Gang Li; Shu-Xia Guo. Use of Blood Lipid Indicators as a Screening Tool of Insulin Resistance among Individuals in Low-Income Country Sides of China: A Multiethnic Region Study. Mediators of Inflammation 2019, 2019, 1 -9.
AMA StyleYi-Zhong Yan, Jia-Ning Fan, Jia-Ming Liu, Yun-Hua Hu, Jiao-Long Ma, Jia He, Heng Guo, Xianghui Zhang, Xin-Ping Wang, Shu-Gang Li, Shu-Xia Guo. Use of Blood Lipid Indicators as a Screening Tool of Insulin Resistance among Individuals in Low-Income Country Sides of China: A Multiethnic Region Study. Mediators of Inflammation. 2019; 2019 ():1-9.
Chicago/Turabian StyleYi-Zhong Yan; Jia-Ning Fan; Jia-Ming Liu; Yun-Hua Hu; Jiao-Long Ma; Jia He; Heng Guo; Xianghui Zhang; Xin-Ping Wang; Shu-Gang Li; Shu-Xia Guo. 2019. "Use of Blood Lipid Indicators as a Screening Tool of Insulin Resistance among Individuals in Low-Income Country Sides of China: A Multiethnic Region Study." Mediators of Inflammation 2019, no. : 1-9.
This study investigated the effects of proanthocyanidins (PC) on arsenic methylation metabolism and efflux in human hepatocytes (L-02), as well as the relationships between PC and GSH, MRP1 and other molecules. Cells were randomly divided into blank control group, arsenic trioxide exposure group (ATO, As2O3, 25μmol/L), and PC-treated arsenic exposure group (10, 25, 50mg/L). After 24/48h, the contents of different forms of arsenic were determined, and the methylation indexes were calculated. Intracellular S-adenosyl methionine (SAM), arsenic (+3 oxidation state) methyltransferase (AS3MT), multidrug resistance-associated protein 1 (MRP1), and reduced glutathione (GSH) were ascertained. Changing trends were observed and the correlation between arsenic metabolism and efflux related factors and arsenic metabolites was analyzed. We observed that cells showed increased levels of content/constituent ratio of methyl arsenic, primary/secondary methylation index, methylation growth efficiency/rate, and the difference of methyl arsenic content in cells and culture medium (P<0.05, resp.). Compared with ATO exposure group, the intracellular SAM content in PC-treated group decreased, and the contents of GSH, AS3MT, and MRP1 increased (P<0.05, resp.). There was a positive correlation between the content of intracellular GSH/AS3MT and methyl arsenic. The content of MRP1 was positively correlated with the difference of methyl arsenic content in cell and culture medium; conversely, the SAM content was negatively correlated with intracellular methyl arsenic content (P<0.05, resp.). Taken together, these results prove that PC can promote arsenic methylation metabolism and efflux in L-02 cells, which may be related to the upregulation of GSH, MRP1, and AS3MT levels by PC.
Qing-Xin Ren; Meng-Chuan Xu; Qiang Niu; Yun-Hua Hu; Hai-Xia Wang; Shu-Gang Li. Effects of Proanthocyanidins on Arsenic Methylation Metabolism and Efflux in Human Hepatocytes L-02. BioMed Research International 2019, 2019, 3924581 -11.
AMA StyleQing-Xin Ren, Meng-Chuan Xu, Qiang Niu, Yun-Hua Hu, Hai-Xia Wang, Shu-Gang Li. Effects of Proanthocyanidins on Arsenic Methylation Metabolism and Efflux in Human Hepatocytes L-02. BioMed Research International. 2019; 2019 ():3924581-11.
Chicago/Turabian StyleQing-Xin Ren; Meng-Chuan Xu; Qiang Niu; Yun-Hua Hu; Hai-Xia Wang; Shu-Gang Li. 2019. "Effects of Proanthocyanidins on Arsenic Methylation Metabolism and Efflux in Human Hepatocytes L-02." BioMed Research International 2019, no. : 3924581-11.
To inform public health policy and research, we analyzed the patterns of life lost to cancers and evaluated the cancer burden in China. Based on the published Chinese Cancer Registry Annual Report and related literature in 2013, we calculated the cancer-related mortality and potential years of life lost (PYLL) by age, sex, districts (urban or rural), to describe the patterns of life lost to cancers. The high death-risk cancers in China were lung, liver, stomach, esophageal, colorectal, breast, pancreatic, brain and nervous system, and ovarian cancers, and leukemia. Liver and esophageal cancers were more prominent among males, while breast and colorectal cancers were more prevalent among females. The most obvious differences of mortality between urban and rural areas were found in liver, esophageal, and colorectal cancers. Cancer-related mortality increased significantly after the age of 30 years, and peaking at 70-79 years. The PYLL rate of cancer in urban areas was higher than that in rural areas (21.49 vs. 19.20/1000), and significant regional and gender differences of PYLL ranks can be observed. For people aged over 60 years, cancer PYLL mainly came from lung, stomach, and esophageal cancers; for middle-aged people, it was mainly induced by liver, colorectal, and female reproductive systems' cancers; and for those under 30 years, life lost to cancer was mainly caused by leukemia and brain, nervous system cancers. Moreover, disparities in age distribution of PYLL from different regions and sexes can be found. In short, three categories of people, including those in urban areas, males and people over 60 years, were suffering from more serious cancer deaths and life lost. These variations pose considerable challenges for the Chinese health care system, and comprehensive measures are required for cancer prevention and treatment.
Yizhong Yan; Yu Chen; Huaimiao Jia; Jiaming Liu; Yusong Ding; Haixia Wang; Yunhua Hu; Jiaolong Ma; Xianghui Zhang; Shugang Li; Yan; Chen; Jia; Liu; Ding; Wang; Hu; Ma; Li. Patterns of Life Lost to Cancers with High Risk of Death in China. International Journal of Environmental Research and Public Health 2019, 16, 2175 .
AMA StyleYizhong Yan, Yu Chen, Huaimiao Jia, Jiaming Liu, Yusong Ding, Haixia Wang, Yunhua Hu, Jiaolong Ma, Xianghui Zhang, Shugang Li, Yan, Chen, Jia, Liu, Ding, Wang, Hu, Ma, Li. Patterns of Life Lost to Cancers with High Risk of Death in China. International Journal of Environmental Research and Public Health. 2019; 16 (12):2175.
Chicago/Turabian StyleYizhong Yan; Yu Chen; Huaimiao Jia; Jiaming Liu; Yusong Ding; Haixia Wang; Yunhua Hu; Jiaolong Ma; Xianghui Zhang; Shugang Li; Yan; Chen; Jia; Liu; Ding; Wang; Hu; Ma; Li. 2019. "Patterns of Life Lost to Cancers with High Risk of Death in China." International Journal of Environmental Research and Public Health 16, no. 12: 2175.
Proanthocyanidin has beneficial features such as free radical scavenging, anti-inflammation, and anti-oxidation. There is no study on whether proanthocyanidin could protect against arsenic-induced respiratory inflammatory damage. The aim of the study is to examine the anti-inflammatory effects of proanthocyanidin and the molecular mechanisms in vivo and in vitro. BEAS-2B cells were treated with As2O3, grape seed proanthocyanidin extract (GSPE), and/or BAY 11–7082. Kunming mice were treated with As2O3 and/or GSPE. p-IκB-α, IκB-α, IKKα/β, NF-κBp65, and NF-κBp50 were assessed by Western blot and qRT-PCR. Lung histology was examined. Arsenic affected the histology of the mouse lungs, but GSPE attenuated those effects. As2O3 increased cell apoptosis, which was reversed by GSPE. In cells and mouse lung tissue, arsenic increased the expression of IL-1β, IL-6, tumor necrosis factor-α, and C-reactive protein, and these effects were attenuated by GSPE. In cells and mouse lung tissue, arsenic enhanced the mRNA and protein levels of IKKα, IKKβ, NF-κBp65, and NF-κBp50, while the IκB-α levels were decreased compared with controls. IKKα, IKKβ, NF-κBp65, and NF-κBp50 mRNA and protein levels in the As2O3+GSPE groups were lower and IκB-α levels were higher than that in the arsenic groups. Arsenic-activated NF-κB signaling induced inflammatory damage through the upregulation of pro-inflammatory cytokines and downregulation of anti-inflammatory cytokines. GSPE plays a beneficial role against arsenic-induced inflammatory damage through, at least in part, the suppression of the arsenic-induced NF-κB signaling pathway. Impact statement Arsenic-induced respiratory inflammatory damage is an important occupational hazard in many areas of the world, particularly in underdeveloped and developing countries. Effective treatments are lacking and expensive. Therefore, the aim of the study was to examine the anti-inflammatory effects of proanthocyanidin (PC) and the molecular mechanisms in vivo and in vitro. The present study showed that PC extracted from grape seed could attenuate the lung damage in a mouse model of arsenic poisoning. The effects were observed at the level of lung histology and inflammasome expression. This study suggests that a natural compound is effective in mitigating the toxic effects of arsenic in the lungs, providing an inexpensive and more readily accessible method for treating arsenic exposure in some parts of the world.
Yunhua Hu; Meng Wei; Qiang Niu; Rulin Ma; Yu Li; Xianhua Wang; Gangling Feng; Shugang Li; Lijuan Pang. Grape seed proanthocyanidin extract alleviates arsenic-induced lung damage through NF-κB signaling. Experimental Biology and Medicine 2019, 244, 213 -226.
AMA StyleYunhua Hu, Meng Wei, Qiang Niu, Rulin Ma, Yu Li, Xianhua Wang, Gangling Feng, Shugang Li, Lijuan Pang. Grape seed proanthocyanidin extract alleviates arsenic-induced lung damage through NF-κB signaling. Experimental Biology and Medicine. 2019; 244 (3):213-226.
Chicago/Turabian StyleYunhua Hu; Meng Wei; Qiang Niu; Rulin Ma; Yu Li; Xianhua Wang; Gangling Feng; Shugang Li; Lijuan Pang. 2019. "Grape seed proanthocyanidin extract alleviates arsenic-induced lung damage through NF-κB signaling." Experimental Biology and Medicine 244, no. 3: 213-226.
Arsenic exposure can cause fibrosis of organs including the liver, heart and lung. It was reported that TGF-β/Smad pathway played a crucial role in the process of fibrosis. However, the mechanism of arsenic-induced fibrosis through TGF-β/Smad signaling pathway has remained controversial. A systematic review and meta-analysis was performed to clarify the relationship between arsenic and TGF-β/Smad pathway, providing a theoretical basis of fibrosis process caused by arsenic. A meta-analysis was used to reveal a correlation between arsenic and fibrosis markers of TGF-β/Smad pathway, including 47 articles of both in vivo and in vitro studies. (Standardized Mean Difference) SMD was employed to compare and analyze the combined effects. When I2 > was 50%, random effect model was selected and subgroup analysis was used to explore the source of heterogeneity. Arsenic exposure up-regulated the expression of TGF-β1, p-Smad2/3, α-SMA, Collagen1/3 and FN. The dose-response relationship showed that low dose (≤5 μmol/L) arsenic exposure up-regulated the expression of TGF-β1, whereas high doses had a tendency to down-regulate that of TGF-β1. Subgroup analysis showed that low or short-term arsenic exposure induced the expression of TGF-β1 and fibrosis markers. The results indicated that arsenic activates the TGF-β/Smad pathway and induced fibrosis. The mechanism is related to the up-regulation of NADPH oxidase and ROS accumulation. However, high-dose arsenic exposure may inhibit this pathway.
Jingyuan Dai; Mengchuan Xu; Xiaoran Zhang; Qiang Niu; Yunhua Hu; Yu Li; Shugang Li. Bi-directional regulation of TGF-β/Smad pathway by arsenic: A systemic review and meta-analysis of in vivo and in vitro studies. Life Sciences 2019, 220, 92 -105.
AMA StyleJingyuan Dai, Mengchuan Xu, Xiaoran Zhang, Qiang Niu, Yunhua Hu, Yu Li, Shugang Li. Bi-directional regulation of TGF-β/Smad pathway by arsenic: A systemic review and meta-analysis of in vivo and in vitro studies. Life Sciences. 2019; 220 ():92-105.
Chicago/Turabian StyleJingyuan Dai; Mengchuan Xu; Xiaoran Zhang; Qiang Niu; Yunhua Hu; Yu Li; Shugang Li. 2019. "Bi-directional regulation of TGF-β/Smad pathway by arsenic: A systemic review and meta-analysis of in vivo and in vitro studies." Life Sciences 220, no. : 92-105.
Purpose. To investigate the effects of grape seed proanthocyanidin extract (GSPE) on oxidative damage and arsenic (As) methylation and to clarify the role of Nrf2 in the process. Methods. L-02 cells were treated with arsenic (25 μM) and GSPE (10, 25, and 50 mg/L) for 24 h. Cell viability was analyzed by MTT assay. Cell apoptosis and ROS fluorescence were detected by flow cytometry. Oxidative stress marker levels were measured using commercial kits. mRNA and protein expression were detected by qRT-PCR and western blotting. The cellular concentrations of methylation products were measured by HPLC-HGAFS. Arsenic methylation ability of cells was determined. Results. Cell survival rate was significantly lower in the As group than in the control group (P<0.05), while cell apoptosis increased and the number of apoptotic cells decreased gradually after GSPE intervention. Superoxide dismutase, glutathione, and sulfhydryl levels in the intervention group were significantly higher (P<0.05), while MDA and ROS levels were significantly lower (P<0.05) than those in the As group. The mRNA and protein expression of Nrf2, HO-1, NQO1, and glutathione-S-transferase increased in the As + GSPE group compared with that in the As group (P<0.05). GSPE significantly increased methylated As level, primary methylation index, secondary methylation index, average growth rate of methylation, and average methylation speed compared with the GSPE untreated group (P<0.05). After Nrf2 inhibition, the effect of GSPE decreased significantly. Conclusion. GSPE activates the Nrf2 signaling pathway to antagonize As-induced oxidative damage and to promote As methylation metabolism. Therefore, GSPE may be a potential agent for relieving As-induced hepatotoxicity.
Mengchuan Xu; Qiang Niu; Yunhua Hu; Gangling Feng; Haixia Wang; Shugang Li. Proanthocyanidins Antagonize Arsenic-Induced Oxidative Damage and Promote Arsenic Methylation through Activation of the Nrf2 Signaling Pathway. Oxidative Medicine and Cellular Longevity 2019, 2019, 1 -19.
AMA StyleMengchuan Xu, Qiang Niu, Yunhua Hu, Gangling Feng, Haixia Wang, Shugang Li. Proanthocyanidins Antagonize Arsenic-Induced Oxidative Damage and Promote Arsenic Methylation through Activation of the Nrf2 Signaling Pathway. Oxidative Medicine and Cellular Longevity. 2019; 2019 ():1-19.
Chicago/Turabian StyleMengchuan Xu; Qiang Niu; Yunhua Hu; Gangling Feng; Haixia Wang; Shugang Li. 2019. "Proanthocyanidins Antagonize Arsenic-Induced Oxidative Damage and Promote Arsenic Methylation through Activation of the Nrf2 Signaling Pathway." Oxidative Medicine and Cellular Longevity 2019, no. : 1-19.
Esophageal squamous cell carcinoma is the most common type of squamous cell carcinoma. Grape seed proanthocyanidin extract (GSPE) is considered to exhibit anticancer activity against several different types of cancer. We aimed to determine whether GSPE inhibited esophageal squamous cancerous cells and the possible involvement of NF-κB in this process. The human esophageal squamous cancer cell line ECA109 was treated with GSPE (0–80 μg/mL) and BAY11-7082 (10 μmol/L) for 12, 24, and 48 h. The MTT assay was used to determine cell proliferation; alterations in cell apoptosis were detected by flow cytometry; levels of inflammatory factors interleukin-6 and cyclooxygenase-2 and apoptotic proteins Bax/Bcl-2 were measured by ELISA; qRT-PCR and western blots were used to examine the activation of caspase-3 and NF-κB signaling. GSPE inhibited the proliferation of ECA109 cells and induced cellular apoptosis in a time- and dose-dependent manner. ELISA results showed that GSPE and BAY11-7082 reduced the secretion of inflammatory cytokines interleukin-6 and cyclooxygenase-2. The results of PCR and western blotting indicated that GSPE and BAY11-7082 activated caspase-3 and attenuated the activation of the NF-κB signaling pathway. GSPE induced apoptosis in ECA109 cells and inhibited ECA109 cell proliferation via a reduction in the secretion of inflammatory cytokines. This mechanism may be related to the attenuation of NF-κB activity and the sensitization of caspase-3.
Fangming Guo; Yunhua Hu; Qiang Niu; Yu Li; Yusong Ding; Rulin Ma; Xianhua Wang; Shugang Li; Jianxin Xie. Grape Seed Proanthocyanidin Extract Inhibits Human Esophageal Squamous Cancerous Cell Line ECA109 via the NF-κB Signaling Pathway. Mediators of Inflammation 2018, 2018, 1 -12.
AMA StyleFangming Guo, Yunhua Hu, Qiang Niu, Yu Li, Yusong Ding, Rulin Ma, Xianhua Wang, Shugang Li, Jianxin Xie. Grape Seed Proanthocyanidin Extract Inhibits Human Esophageal Squamous Cancerous Cell Line ECA109 via the NF-κB Signaling Pathway. Mediators of Inflammation. 2018; 2018 ():1-12.
Chicago/Turabian StyleFangming Guo; Yunhua Hu; Qiang Niu; Yu Li; Yusong Ding; Rulin Ma; Xianhua Wang; Shugang Li; Jianxin Xie. 2018. "Grape Seed Proanthocyanidin Extract Inhibits Human Esophageal Squamous Cancerous Cell Line ECA109 via the NF-κB Signaling Pathway." Mediators of Inflammation 2018, no. : 1-12.
Regulated in development and DNA damage response (REDD1), a gene responding to hypoxia or multiple DNA damage events, was recently implicated in cancer development and progression. Previously, in vivo and in vitro experiments indicated that REDD1 functions as an oncogene in ovarian cancer cells. However, the role of REDD1 in cancer cell migration and invasion and in clinical significance of prognostic values is not examined in detail. We detected the REDD1 protein expression by immunohistochemistry in 18 normal ovarian surface epithelium or fallopian tube epithelium specimens, 24 ovarian borderline tumors, and 229 ovarian cancers. Fisher's exact test, logistic regression analysis, the Kaplan-Meier method, and the log-rank test were used to evaluate the association of REDD1 with clinical factors, overall survival and disease-free survival. The prognostic predictive value of REDD1 for ovarian cancer patients was evaluated using multivariate Cox proportional hazard regression models. REDD1 expression in HEY, HEY A8, SKOV3, SKOV3 ip1, OVCA429, OVCA433 and A2780 human ovarian epithelial cancer cell lines was detected by western blotting. The role of REDD1 in cell invasion and migration was assessed by transwell migration and invasion assays using SKOV3, A2780, HEY, HEYA8, and SKOV3-REDD1 with parental A2780-REDD1 HEY-REDD1i and HEY A8-REDD1i. High expression of REDD1 was observed in 35.4% of primary ovarian carcinoma samples. Overexpression of cytoplasmic REDD1 in ovarian cancer was significantly associated with serous carcinoma (P < 0.001), late-stage disease (P < 0.001), ascites (P < 0.001), and partial or non-response to chemotherapy (P < 0.001). High cytoplasmic expression of REDD1 was correlated with poorer overall survival (P < 0.001) and disease-free survival (P < 0.001). The multivariate Cox proportional hazards regression analysis indicated that patients with high cytoplasmic REDD1 expression had a high risk of death (P < 0.001) and high risk of an event (i.e., recurrence, progression, or death) (P < 0.001). REDD1 was first reported as an independent prognostic factor in ovarian cancer patients. In addition, REDD1 overexpression enhanced ovarian cancer cell migration and invasion. REDD1 is an independent unfavorable prognostic factor in ovarian carcinoma and may promote ovarian cancer metastasis.
Bin Chang; Jiao Meng; Huimin Zhu; Xiang Du; Lili Sun; Lei Wang; Shugang Li; Gong Yang. Overexpression of the recently identified oncogene REDD1 correlates with tumor progression and is an independent unfavorable prognostic factor for ovarian carcinoma. Diagnostic Pathology 2018, 13, 87 .
AMA StyleBin Chang, Jiao Meng, Huimin Zhu, Xiang Du, Lili Sun, Lei Wang, Shugang Li, Gong Yang. Overexpression of the recently identified oncogene REDD1 correlates with tumor progression and is an independent unfavorable prognostic factor for ovarian carcinoma. Diagnostic Pathology. 2018; 13 (1):87.
Chicago/Turabian StyleBin Chang; Jiao Meng; Huimin Zhu; Xiang Du; Lili Sun; Lei Wang; Shugang Li; Gong Yang. 2018. "Overexpression of the recently identified oncogene REDD1 correlates with tumor progression and is an independent unfavorable prognostic factor for ovarian carcinoma." Diagnostic Pathology 13, no. 1: 87.
Arsenic is known to cause oxidative damage. Nuclear factor E2-relate factor-2 (Nrf2) can resist this toxicity. Scholars demonstrated that Nrf2 pathway was activated by arsenic. In contrast, other articles established arsenic-induced inhibition of Nrf2 pathway. To resolve the contradiction and elucidate the mechanism of Nrf2 induced by arsenic, 39 publications involving mouse models were identified through exhaustive database retrieval and were analyzed. The pooled results suggested that arsenic obviously elevated transcription and translation levels of Nrf2 and its downstream genes, NAD(P)H dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1), glutamate-cysteine ligase catalytic subunit (GCLC), and GST-glutathione-S-transferase1/2 (GSTO1/2). Arsenic increased the level of reactive oxygen species (ROS), but reduced the level of glutathione (GSH). Subgroup analysis between arsenic and control groups showed that the levels of Nrf2 and its downstream genes are greater in high dose than that in the low dose, higher in short-term exposure than long term, female subjects tolerated better than males, higher in mice than the rats, and greater in other organs than the liver. However, the contents of genes of Nrf2 pathway between the arsenic and control groups were lower in rats than in mice and were less for long-term exposure than the short term (P < 0.05). Conclusively, a variable regulation of arsenic on Nrf2 pathway is noted. Higher dose and short-term exposure of female mice organs except for liver promoted Nrf2 pathway. On the other hand, arsenic inhibited Nrf2 pathway for long-term exposure on rats.
Cheng Wang; Qiang Niu; Rulin Ma; Guanling Song; Yunhua Hu; Shangzhi Xu; Yu Li; Haixia Wang; Shugang Li; Yusong Ding. The Variable Regulatory Effect of Arsenic on Nrf2 Signaling Pathway in Mouse: a Systematic Review and Meta-analysis. Biological Trace Element Research 2018, 190, 362 -383.
AMA StyleCheng Wang, Qiang Niu, Rulin Ma, Guanling Song, Yunhua Hu, Shangzhi Xu, Yu Li, Haixia Wang, Shugang Li, Yusong Ding. The Variable Regulatory Effect of Arsenic on Nrf2 Signaling Pathway in Mouse: a Systematic Review and Meta-analysis. Biological Trace Element Research. 2018; 190 (2):362-383.
Chicago/Turabian StyleCheng Wang; Qiang Niu; Rulin Ma; Guanling Song; Yunhua Hu; Shangzhi Xu; Yu Li; Haixia Wang; Shugang Li; Yusong Ding. 2018. "The Variable Regulatory Effect of Arsenic on Nrf2 Signaling Pathway in Mouse: a Systematic Review and Meta-analysis." Biological Trace Element Research 190, no. 2: 362-383.
Synovial sarcoma (SS) is a highly aggressive malignant soft tissue sarcoma with typical characteristics of both epithelial and mesenchymal differentiation. Matrix metalloproteinase-14 (MMP-14) is reported to play an important role in some of these tumors. It induces epithelial-to-mesenchymal transition (EMT) in some carcinomas, such as breast and prostate cancers. However, the role of MMP-14 in the pathogenesis of SS remains unclear. Therefore, we investigated the role of MMP-14 and EMT/mesenchymal-to-epithelial transition (MET) in SS. The expression of MMP-14 and EMT-related proteins was determined in 37 SS cases and transfected cells by immunohistochemistry staining and Western blotting. The invasion ability of transfected cells was determined by transwell invasion assay. The expression rates of MMP-14, E-cadherin, N-cadherin, and vimentin were 75.7%, 54.1%, 75.7%, and 100%, respectively, in the cases of SS. The expression of MMP-14 correlated negatively with E-cadherin and positively with N-cadherin in monophasic fibrous SS. The MMP-14 protein expression was higher in stage III/IV than in stage I/II. After MMP-14 was transfected into SW982 cells, MMP-14, N-cadherin, and vimentin expression was upregulated, and E-cadherin expression was downregulated. High expression of MMP-14 enhanced the invasive ability of SW982 cells. Our findings suggest that MMP-14 enhances the invasive ability of SW982 cells by inducing EMT. By this action, it may play an important role in the occurrence and development of SS.
Manli Liu; Yan Qi; Lili Zhao; Dongdong Chen; Yang Zhou; Hongrun Zhou; Yanmin Lv; Lu Zhang; Shan Jin; Shugang Li; Hong Zou; Wei Jia; Cuicui Wang; Jinfang Jiang; Weihua Liang; Lijuan Pang; Feng Li. Matrix metalloproteinase-14 induces epithelial-to-mesenchymal transition in synovial sarcoma. Human Pathology 2018, 80, 201 -209.
AMA StyleManli Liu, Yan Qi, Lili Zhao, Dongdong Chen, Yang Zhou, Hongrun Zhou, Yanmin Lv, Lu Zhang, Shan Jin, Shugang Li, Hong Zou, Wei Jia, Cuicui Wang, Jinfang Jiang, Weihua Liang, Lijuan Pang, Feng Li. Matrix metalloproteinase-14 induces epithelial-to-mesenchymal transition in synovial sarcoma. Human Pathology. 2018; 80 ():201-209.
Chicago/Turabian StyleManli Liu; Yan Qi; Lili Zhao; Dongdong Chen; Yang Zhou; Hongrun Zhou; Yanmin Lv; Lu Zhang; Shan Jin; Shugang Li; Hong Zou; Wei Jia; Cuicui Wang; Jinfang Jiang; Weihua Liang; Lijuan Pang; Feng Li. 2018. "Matrix metalloproteinase-14 induces epithelial-to-mesenchymal transition in synovial sarcoma." Human Pathology 80, no. : 201-209.
Xinping Wang; Heng Guo; Yu Li; Haixia Wang; Jia He; Lati Mu; Yunhua Hu; Jiaolong Ma; Yizhong Yan; Shugang Li; Yusong Ding; Mei Zhang; Qiang Niu; Jiaming Liu; Jingyu Zhang; Rulin Ma; Shuxia Guo. untitled protocol v1 (protocols.io.mmtc46n). protocols.io 2018, 1 .
AMA StyleXinping Wang, Heng Guo, Yu Li, Haixia Wang, Jia He, Lati Mu, Yunhua Hu, Jiaolong Ma, Yizhong Yan, Shugang Li, Yusong Ding, Mei Zhang, Qiang Niu, Jiaming Liu, Jingyu Zhang, Rulin Ma, Shuxia Guo. untitled protocol v1 (protocols.io.mmtc46n). protocols.io. 2018; ():1.
Chicago/Turabian StyleXinping Wang; Heng Guo; Yu Li; Haixia Wang; Jia He; Lati Mu; Yunhua Hu; Jiaolong Ma; Yizhong Yan; Shugang Li; Yusong Ding; Mei Zhang; Qiang Niu; Jiaming Liu; Jingyu Zhang; Rulin Ma; Shuxia Guo. 2018. "untitled protocol v1 (protocols.io.mmtc46n)." protocols.io , no. : 1.
Arsenic is a toxic metal, which ultimately leads to cell apoptosis. ERK is considered a key transcriptional regulator of arsenic-induced apoptosis. Due to a few controversial issues about arsenic-mediated extracellular signal-regulated MAP kinases (ERK) signaling, a meta-analysis was performed. Subgroup analyses demonstrated that high doses (≥2 µmol/l) of arsenic increased the expression of Ras, ERK, ERK1, ERK2, phosphorylated (p)-ERK, p-ERK1, and p-ERK2, while low doses (24 h) to arsenic led to inhibition of expression of ERK1, p-ERK1, and p-ERK2, whereas short-term exposure (≤24 h) triggered the expression of ERK1, ERK2, p-ERK, p-ERK1, and p-ERK2. Furthermore, normal cells exposed to arsenic exhibited higher production levels of Ras and p-ERK. Conversely, exposure of cancer cells to arsenic showed a lower level of production of Ras and p-ERK as well as higher level of p-ERK1 and p-ERK2 as compared to control group. Short-term exposure of normal cells to high doses of arsenic may promote ERK signaling pathway. In contrast, long-term exposure of cancer cells to low doses of arsenic may inhibit ERK signaling pathway. This study may be helpful in providing a theoretical basis for the diverging result of arsenic adverse effects on one hand and therapeutic mechanisms on the other concerning arsenic-induced apoptosis.
Dongjie Li; Yutao Wei; Shangzhi Xu; Qiang Niu; Mei Zhang; Shugang Li; Mingxia Jing. A systematic review and meta-analysis of bidirectional effect of arsenic on ERK signaling pathway. Molecular Medicine Reports 2018, 17, 4422 -4432.
AMA StyleDongjie Li, Yutao Wei, Shangzhi Xu, Qiang Niu, Mei Zhang, Shugang Li, Mingxia Jing. A systematic review and meta-analysis of bidirectional effect of arsenic on ERK signaling pathway. Molecular Medicine Reports. 2018; 17 (3):4422-4432.
Chicago/Turabian StyleDongjie Li; Yutao Wei; Shangzhi Xu; Qiang Niu; Mei Zhang; Shugang Li; Mingxia Jing. 2018. "A systematic review and meta-analysis of bidirectional effect of arsenic on ERK signaling pathway." Molecular Medicine Reports 17, no. 3: 4422-4432.
Aims: Esophageal squamous cell carcinoma (ESCC) is characterized by high prevalence and mortality worldwide, and it is very highly prevalent in China. ESCC is caused by various factors, including microRNAs (miRNAs) whose expression have been shown to play a major role in tumor generation. Single nucleotide polymorphisms (SNPs) in miRNAs could affect susceptibility to numerous cancers. This study aimed to evaluate the relationship between SNPs in miR-124 and ESCC risk in the Chinese Kazakh population. Methods: A total of 239 Chinese Kazakh patients with ESCC and 227 healthy Chinese Kazakh individuals were recruited in this study. Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry was used to analyze the miR-124 rs531564 genotype. Results: Allele G of the miR-124 rs531564 polymorphism significantly reduced the risk of ESCC in the Chinese Kazakh population [odds ratio (OR) = 0.711; 95% confidence interval (CI): 0.508–0.996; p = 0.047]. The dominant model indicated that the CG+GG genotypes were associated with significantly decreased ESCC risk compared to the CC genotype (adjusted OR = 0.586; 95% CI: 0.396–0.867; p = 0.007). Stratification analyses showed that compared with the CC genotype, the CG and CG+GG genotypes manifested reduced ESCC risks in the female group [CG vs. CC: OR = 0.472; 95% CI: 0.255–0.872; p = 0.016; (CG+GG) vs. CC: OR = 0.472; 95% CI: 0.255–0.872; p = 0.016] and the age group of <57 years old [CG vs. CC: OR = 0.456; 95% CI: 0.258–0.806; p = 0.006; (CG+GG) vs. CC: OR = 0.456; 95%CI: 0.258–0.806; p = 0.006]. The miR-124 rs531564 polymorphism showed no significant association with histological stage, lymph node metastasis, depth of invasion, or tumor/node/metastasis stage. Conclusions: Our findings are the first to be reported that the miR-124 rs531564 polymorphism decreased ESCC risk in the Chinese Kazakh population.
Fei Wu; Mei Li; Weiyan You; Yu Ji; Xiaobin Cui; Jianming Hu; Yunzhao Chen; Lijuan Pang; Shugang Li; Yutao Wei; Lan Yang; Feng Li. A Genetic Variant in miR-124 Decreased the Susceptibility to Esophageal Squamous Cell Carcinoma in a Chinese Kazakh Population. Genetic Testing and Molecular Biomarkers 2018, 22, 29 -34.
AMA StyleFei Wu, Mei Li, Weiyan You, Yu Ji, Xiaobin Cui, Jianming Hu, Yunzhao Chen, Lijuan Pang, Shugang Li, Yutao Wei, Lan Yang, Feng Li. A Genetic Variant in miR-124 Decreased the Susceptibility to Esophageal Squamous Cell Carcinoma in a Chinese Kazakh Population. Genetic Testing and Molecular Biomarkers. 2018; 22 (1):29-34.
Chicago/Turabian StyleFei Wu; Mei Li; Weiyan You; Yu Ji; Xiaobin Cui; Jianming Hu; Yunzhao Chen; Lijuan Pang; Shugang Li; Yutao Wei; Lan Yang; Feng Li. 2018. "A Genetic Variant in miR-124 Decreased the Susceptibility to Esophageal Squamous Cell Carcinoma in a Chinese Kazakh Population." Genetic Testing and Molecular Biomarkers 22, no. 1: 29-34.
Emerging evidence has demonstrated that iron overload plays an important role in oxidative stress in the liver. This study aimed to explore whether fluoride-induced hepatic oxidative stress is associated with iron overload and whether grape seed proanthocyanidin extract (GSPE) alleviates oxidative stress by reducing iron overload. Forty Kunming male mice were randomly divided into 4 groups and treated for 5 weeks with distilled water (control), sodium fluoride (NaF) (100 mg/L), GSPE (400 mg/kg bw), or NaF (100 mg/L) + GSPE (400 mg/kg bw). Mice exposed to NaF showed typical poisoning changes of morphology, increased aspartate aminotransferase and alanine aminotransferase activities in the liver. NaF treatment also increased MDA accumulation, decreased GSH-Px, SOD and T-AOC levels in liver, indicative of oxidative stress. Intriguingly, all these detrimental effects were alleviated by GSPE. Further study revealed that NaF induced disorders of iron metabolism, as manifested by elevated iron level with increased hepcidin but decreased ferroportin expression, which contributed to hepatic oxidative stress. Importantly, the iron dysregulation induced by NaF could be normalized by GSPE. Collectively, these data provide a novel insight into mechanisms underlying fluorosis and highlight the potential of GSPE as a naturally occurring prophylactic treatment for fluoride-induced hepatotoxicity associated with iron overload.
Qiang Niu; Ping He; Shangzhi Xu; Ruling Ma; Yusong Ding; Lati Mu; Shugang Li. Fluoride-induced iron overload contributes to hepatic oxidative damage in mouse and the protective role of Grape seed proanthocyanidin extract. The Journal of Toxicological Sciences 2018, 43, 311 -319.
AMA StyleQiang Niu, Ping He, Shangzhi Xu, Ruling Ma, Yusong Ding, Lati Mu, Shugang Li. Fluoride-induced iron overload contributes to hepatic oxidative damage in mouse and the protective role of Grape seed proanthocyanidin extract. The Journal of Toxicological Sciences. 2018; 43 (5):311-319.
Chicago/Turabian StyleQiang Niu; Ping He; Shangzhi Xu; Ruling Ma; Yusong Ding; Lati Mu; Shugang Li. 2018. "Fluoride-induced iron overload contributes to hepatic oxidative damage in mouse and the protective role of Grape seed proanthocyanidin extract." The Journal of Toxicological Sciences 43, no. 5: 311-319.
The clinicopathological effects of Bmi-1 expression in esophageal cancer remain widely disputed. Our aim was to clarify this relationship.Available studies were retrieved from diverse databases. Review Manager 5.3 and Stata 12.0 software were used to identify correlations between Bmi-1 expression and the clinicopathological features of esophageal cancer.From 16 studies, 1523 esophageal cancer patients were analyzed. Meta-analysis demonstrated that Bmi-1 overexpression was associated with differentiation (p = 0.03), tumor/node/metastasis stage (p = 0.02), depth of invasion (p = 0.0006) and lymph node metastasis (p = 0.008).The expression of Bmi-1 is associated with the progression and invasion of esophageal cancer.
Jihong Liu; Kai Liu; Xianli Jiang; Xueli Wang; Yunzhao Chen; Xiaobin Cui; Lijuan Pang; Shugang Li; Chunxia Liu; Hong Zou; Lan Yang; Jin Zhao; Yan Qi; Jian Ming Hu; Feng Li. Clinicopathological significance of Bmi-1 overexpression in esophageal cancer: a meta-analysis. Biomarkers in Medicine 2018, 12, 71 -81.
AMA StyleJihong Liu, Kai Liu, Xianli Jiang, Xueli Wang, Yunzhao Chen, Xiaobin Cui, Lijuan Pang, Shugang Li, Chunxia Liu, Hong Zou, Lan Yang, Jin Zhao, Yan Qi, Jian Ming Hu, Feng Li. Clinicopathological significance of Bmi-1 overexpression in esophageal cancer: a meta-analysis. Biomarkers in Medicine. 2018; 12 (1):71-81.
Chicago/Turabian StyleJihong Liu; Kai Liu; Xianli Jiang; Xueli Wang; Yunzhao Chen; Xiaobin Cui; Lijuan Pang; Shugang Li; Chunxia Liu; Hong Zou; Lan Yang; Jin Zhao; Yan Qi; Jian Ming Hu; Feng Li. 2018. "Clinicopathological significance of Bmi-1 overexpression in esophageal cancer: a meta-analysis." Biomarkers in Medicine 12, no. 1: 71-81.
This meta-analysis was conducted to evaluate the association of CD133 and Nestin with epithelial ovarian cancer. Databases (PubMed, EMBASE, Web of Science, China National Knowledge Infrastructure, Wanfang) were searched for relevant studies updated in August 2017. CD133 and Nestin expression were estimated by immunohistochemistry. Statistical analysis was performed by RevMan. A total of 18 studies were included in this meta-analysis. High expression of both CD133 and Nestin was associated with late International Federation of Gynecology and Obstetrics stage (p < 0.00001), larger size of residual cancer (p < 0.05). CD133 overexpression was also associated with higher histological grade (p = 0.0006) and lymph node metastases (p < 0.00001). Nestin overexpression was associated with a higher rate of treatment resistance (p = 0.0007). Positive expression of CD133 and Nestin may be associated with aggressive biological behaviors in epithelial ovarian cancer.
Lili Zhao; Jun Li; Manli Liu; Hongrun Zhou; Hong Zou; Yutao Wei; Kunming Sun; Ganxiong Li; Shugang Li; Lijuan Pang. The clinicopathological parameters significance of CD133 and Nestin in epithelial ovarian cancer: a meta-analysis. Future Oncology 2017, 13, 2555 -2570.
AMA StyleLili Zhao, Jun Li, Manli Liu, Hongrun Zhou, Hong Zou, Yutao Wei, Kunming Sun, Ganxiong Li, Shugang Li, Lijuan Pang. The clinicopathological parameters significance of CD133 and Nestin in epithelial ovarian cancer: a meta-analysis. Future Oncology. 2017; 13 (28):2555-2570.
Chicago/Turabian StyleLili Zhao; Jun Li; Manli Liu; Hongrun Zhou; Hong Zou; Yutao Wei; Kunming Sun; Ganxiong Li; Shugang Li; Lijuan Pang. 2017. "The clinicopathological parameters significance of CD133 and Nestin in epithelial ovarian cancer: a meta-analysis." Future Oncology 13, no. 28: 2555-2570.
This study aims to investigate association between six single nucleotide polymorphisms(SNPs) in APOA1 gene and types of obesity with the risk of low level HDL-C in the pastoral area of northwest China. A total of 1267 individuals including 424 patients with low HDL-C disease and 843 health subjects were analyzed based on matched for age, sex. SNPShot technique was used to detect the genotypes of rs670, rs5069, rs5072, rs7116797, rs2070665 and rs1799837 in APOA1 gene. The relationship between above six SNPs and types of obesity with low HDL-C disease was analyzed by binary logistic regression. Carriers with rs670 G allele were more likely to get low HDL-C disease (OR = 1.46, OR95%CI: 1.118–1.915; P = 0.005); The genotypic and allelic frequencies of rs5069, rs5072, rs7116797, rs2070665, rs1799837 revealed no significant differences between cases and controls (P < 0.05); with reference to normal weight, Waist circumference (WC), Waist-to-hip ratio (WHR) individuals, respectively, general obesity measured by BMI had 2.686 times (OR95%CI: 1.695–4.256; P < 0.01), abdominal obesity measured by WC had 1.925 times (OR95%CI: 1.273–2.910; P = 0.002) and abdominal obesity measured by WHR had 1.640 times (OR95%CI: 1.114–2.416; P = 0.012) risk to get low HDL-C disease; APOA1 rs670 interacted with obesity (no matter general obesity or abdominal obesity) on low HDL-C disease. APOA1 gene may be associated with low HDL-C disease in the pastoral area of northwest China; obesity was the risk factor for low HDL-C disease; the low HDL-C disease is influenced by APOA1, obesity, and their interactions.
Xinping Wang; Jia He; Heng Guo; Lati Mu; Yunhua Hu; Jiaolong Ma; Yizhong Yan; Rulin Ma; Shugang Li; Yusong Ding; Mei Zhang; Qiang Niu; Jiaming Liu; Jingyu Zhang; Shuxia Guo. Interactions of six SNPs in APOA1 gene and types of obesity on low HDL-C disease in Xinjiang pastoral area of China. Lipids in Health and Disease 2017, 16, 187 -187.
AMA StyleXinping Wang, Jia He, Heng Guo, Lati Mu, Yunhua Hu, Jiaolong Ma, Yizhong Yan, Rulin Ma, Shugang Li, Yusong Ding, Mei Zhang, Qiang Niu, Jiaming Liu, Jingyu Zhang, Shuxia Guo. Interactions of six SNPs in APOA1 gene and types of obesity on low HDL-C disease in Xinjiang pastoral area of China. Lipids in Health and Disease. 2017; 16 (1):187-187.
Chicago/Turabian StyleXinping Wang; Jia He; Heng Guo; Lati Mu; Yunhua Hu; Jiaolong Ma; Yizhong Yan; Rulin Ma; Shugang Li; Yusong Ding; Mei Zhang; Qiang Niu; Jiaming Liu; Jingyu Zhang; Shuxia Guo. 2017. "Interactions of six SNPs in APOA1 gene and types of obesity on low HDL-C disease in Xinjiang pastoral area of China." Lipids in Health and Disease 16, no. 1: 187-187.
A long-term exposure to arsenic may lead to lung damage due to oxidative stress. In this context, GSPE can play a major role as a strong antioxidant. Our study attempted to reveal the connection between arsenic-induced lung injury and the antagonistic effect of GSPE. For this purpose, BEAS-2B cells and Kunming mice were exposed to different dosages of As2O3 and GSPE. Oxidative stress indicators were detected both in vivo and in vitro. Cell survival rate and morphological changes in the lung tissue (H&E staining) were evaluated as well. It was exhibited that As2O3 increased oxidative stress both in vivo and in vitro and decreased cells viability. In contrast, higher cell survival rate was revealed in the group treated with arsenic plus GSPE after 24 h as compared to that in the arsenic group. GSPE effectively reduced oxidative stress levels, along with increasing antioxidant capacity. In vivo experiments in arsenic-exposed group showed alveolar septum to be significantly thickened with considerable capillary congestion and invasion by inflammatory cells. After the intervention with GSPE, there seemed to be a dramatic reversal of morphology with thinning of the alveolar septum, decrease in capillary congestion, and number of inflammatory cells. This had shown that GSPE can effectively reduce the levels of oxidative stress, induced by arsenic in mice lung tissue. Conversely, antioxidant enzymes or products were increased. The experiment proved that GSPE can protect the lungs from oxidative damage induced by arsenic, and it may also be used as an antagonist against arsenic injuries.
Meng Wei; Fangming Guo; Dongsheng Rui; Haixia Wang; Gangling Feng; Shugang Li; Guanling Song. Alleviation of Arsenic-Induced Pulmonary Oxidative Damage by GSPE as Shown during In vivo and In vitro Experiments. Biological Trace Element Research 2017, 183, 80 -91.
AMA StyleMeng Wei, Fangming Guo, Dongsheng Rui, Haixia Wang, Gangling Feng, Shugang Li, Guanling Song. Alleviation of Arsenic-Induced Pulmonary Oxidative Damage by GSPE as Shown during In vivo and In vitro Experiments. Biological Trace Element Research. 2017; 183 (1):80-91.
Chicago/Turabian StyleMeng Wei; Fangming Guo; Dongsheng Rui; Haixia Wang; Gangling Feng; Shugang Li; Guanling Song. 2017. "Alleviation of Arsenic-Induced Pulmonary Oxidative Damage by GSPE as Shown during In vivo and In vitro Experiments." Biological Trace Element Research 183, no. 1: 80-91.