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Prof. Shuhua Yang
Key Laboratory of Zoonosis of Liaoning Province

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Research article
Published: 05 January 2021 in Oxidative Medicine and Cellular Longevity
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Ochratoxin A (OTA) is a common environmental pollutant found in a variety of foods and grains, and excessive OTA consumption causes serious global health effects on animals and humans. Astaxanthin (AST) is a natural carotenoid that has anti-inflammatory, antiapoptotic, immunomodulatory, antitumor, antidiabetes, and other biological activities. The present study is aimed at investigating the effects of AST on OTA-induced cecum injury and its mechanism of action. Eighty C57 mice were randomly divided into four groups, including the control group, OTA group (5 mg/kg body weight), AST group (100 mg/kg body weight), and AST intervention group (100 mg/kg body weight AST+5 mg/kg body weight OTA). It was found that AST decreased the endotoxin content, effectively prevented the shortening of mouse cecum villi, and increased the expression levels of tight junction (TJ) proteins, consisting of occludin, claudin-1, and zonula occludens-1 (ZO-1). AST increased the number of goblet cells, the contents of mucin-2 (MUC2), and defensins (Defa5 and β-pD2) significantly, while the expression of mucin-1 (MUC1) decreased significantly. The 16S rRNA sequencing showed that AST affected the richness and diversity of cecum flora, decreased the proportion of lactobacillus, and also decreased the contents of short-chain fatty acids (SCFAs) (acetate and butyrate). In addition, AST significantly decreased the expression of TLR4, MyD88, and p-p65, while increasing the expression of p65. Meanwhile, the expression of inflammatory factors including TNF-α and INF-γ decreased, while the expression of IL-10 increased. In conclusion, AST reduced OTA-induced cecum injury by regulating the cecum barrier function and TLR4/MyD88/NF-κB signaling pathway.

ACS Style

Yueli Chen; Shiwei Zhao; Danyang Jiao; Beibei Yao; Shuhua Yang; Peng Li; Miao Long. Astaxanthin Alleviates Ochratoxin A-Induced Cecum Injury and Inflammation in Mice by Regulating the Diversity of Cecal Microbiota and TLR4/MyD88/NF-κB Signaling Pathway. Oxidative Medicine and Cellular Longevity 2021, 2021, 1 -13.

AMA Style

Yueli Chen, Shiwei Zhao, Danyang Jiao, Beibei Yao, Shuhua Yang, Peng Li, Miao Long. Astaxanthin Alleviates Ochratoxin A-Induced Cecum Injury and Inflammation in Mice by Regulating the Diversity of Cecal Microbiota and TLR4/MyD88/NF-κB Signaling Pathway. Oxidative Medicine and Cellular Longevity. 2021; 2021 ():1-13.

Chicago/Turabian Style

Yueli Chen; Shiwei Zhao; Danyang Jiao; Beibei Yao; Shuhua Yang; Peng Li; Miao Long. 2021. "Astaxanthin Alleviates Ochratoxin A-Induced Cecum Injury and Inflammation in Mice by Regulating the Diversity of Cecal Microbiota and TLR4/MyD88/NF-κB Signaling Pathway." Oxidative Medicine and Cellular Longevity 2021, no. : 1-13.

Journal article
Published: 08 May 2020 in Food and Chemical Toxicology
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Zearalenone (ZEA) is a mycotoxin that contaminates crops worldwide and is toxic to the reproductive systems of mammals, however, the toxicological mechanism by which ZEA affects germ cells is not fully understood. In this study, proteomic analysis using iTRAQ technology was adopted to determine the cellular response of Leydig cells of rats to ZEA exposure. The results were used to elucidate the mechanisms responsible for the toxicity of the ZEA towards germ cells. After 24 h of exposure to ZEA at a concentration of 30 μmol/L, a total of 128 differentially expressed proteins (DEPs) were identified. Of these, 70 DEPs were up-regulated and 58 DEPs were down-regulated. The DEPs associated with ZEA toxicology were then screened by using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. The results show that these DEPs are involved in a number of important ZEA toxicological pathways including apoptosis, immunotoxicity, DNA damage, and signaling pathways. The complex regulatory relationships between the DEPs and ZEA toxicological signaling pathways are also explicitly demonstrated in the form of a protein–protein interaction network. This study thus provides a theoretical molecular basis for understanding the toxicological mechanisms by which ZEA affects germ cells.

ACS Style

Mingyang Wang; Shuhua Yang; Jing Cai; Rong Yan; Lingqi Meng; Miao Long; Yi Zhang. Proteomic analysis using iTRAQ technology reveals the toxic effects of zearalenone on the leydig cells of rats. Food and Chemical Toxicology 2020, 141, 111405 .

AMA Style

Mingyang Wang, Shuhua Yang, Jing Cai, Rong Yan, Lingqi Meng, Miao Long, Yi Zhang. Proteomic analysis using iTRAQ technology reveals the toxic effects of zearalenone on the leydig cells of rats. Food and Chemical Toxicology. 2020; 141 ():111405.

Chicago/Turabian Style

Mingyang Wang; Shuhua Yang; Jing Cai; Rong Yan; Lingqi Meng; Miao Long; Yi Zhang. 2020. "Proteomic analysis using iTRAQ technology reveals the toxic effects of zearalenone on the leydig cells of rats." Food and Chemical Toxicology 141, no. : 111405.

Journal article
Published: 26 April 2020 in Food and Chemical Toxicology
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The toxic effect of zearalenone (ZEA) is not fully understood and there is an urgent need for the development of effective agents to protect against the toxic effects of ZEA. In this study, we detected whether curcumin (CUR) can reduce Leydig cells apoptosis induced by ZEA. The Effects of ZEA and CUR on cell viability was evaluated using a Cell Counting kit-8 assay (CCK-8). Apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and flow cytometry. The protective effect of CUR on oxidative stress induced by ZEA was determined by ROS, MDA, T-SOD, GSH and GSH-Px levels. In addition, we also determined effects of key signaling pathways and proteins involved in the apoptotic, PI3K-AKT, Nrf2 and endoplasmic reticulum stress signaling pathways by Western blotting. The expressions of proteins (PTEN, AKT, p-AKT, Bax, Bcl-2, GRP78, CHOP, JNK, P-JNK, Caspase-12, Caspase-9, Caspase-3, Nrf2, Keap1 and HO-1) were measured. The experimental results showed that CUR can alleviate oxidative stress and apoptosis caused by ZEA through the PI3K-AKT, Nrf2 and endoplasmic reticulum stress signaling pathways. Our results provide a theoretical basis for molecular studies of ZEA toxicology and clinical application of CUR.

ACS Style

Si Chen; Shuhua Yang; Mingyang Wang; Jia Chen; Sheng Huang; Zhen Wei; Ziyang Cheng; Hanli Wang; Miao Long; Peng Li. Curcumin inhibits zearalenone-induced apoptosis and oxidative stress in Leydig cells via modulation of the PTEN/Nrf2/Bip signaling pathway. Food and Chemical Toxicology 2020, 141, 111385 .

AMA Style

Si Chen, Shuhua Yang, Mingyang Wang, Jia Chen, Sheng Huang, Zhen Wei, Ziyang Cheng, Hanli Wang, Miao Long, Peng Li. Curcumin inhibits zearalenone-induced apoptosis and oxidative stress in Leydig cells via modulation of the PTEN/Nrf2/Bip signaling pathway. Food and Chemical Toxicology. 2020; 141 ():111385.

Chicago/Turabian Style

Si Chen; Shuhua Yang; Mingyang Wang; Jia Chen; Sheng Huang; Zhen Wei; Ziyang Cheng; Hanli Wang; Miao Long; Peng Li. 2020. "Curcumin inhibits zearalenone-induced apoptosis and oxidative stress in Leydig cells via modulation of the PTEN/Nrf2/Bip signaling pathway." Food and Chemical Toxicology 141, no. : 111385.

Journal article
Published: 18 March 2020 in Food and Chemical Toxicology
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Fumonisin B1 (FB1) is a mycotoxin that contaminates cash crops and has toxic effects on humans and livestock. However, the toxic effect of FB1 is not fully understood. In this study, the apoptosis mechanism of FB1 on porcine kidney cells (PK-15) was elucidated by transcriptome analysis. The results showed that FB1 observably changed the expression of mRNA in PK-15 and induced the cells of apoptosis after being exposed to 106 μM FB1 in vitro. Gene Ontology and KEGG enrichment analyses showed that FB1 exposure increased the expressions of related mRNA in TNF signalling pathway in PK-15. To verify our bioinformatics analysis, these changes were verified by qRT-PCR and Western blot assay. Furthermore, the mRNA expressions of NF-κB and its downstream genes or proteins decreased significantly (p < 0.01) after the addition of BAY11-7082, the inhibitor of NF-κB. Therefore, for the first time, we demonstrate that FB1 can induce apoptosis of PK-15 cells through TNF signalling pathway, and NF-κB gene is a target of FB1 acting on the TNF signalling pathway.

ACS Style

Jia Chen; Shuhua Yang; Sheng Huang; Rong Yan; Mingyang Wang; Si Chen; Jing Cai; Miao Long; Peng Li. Transcriptome study reveals apoptosis of porcine kidney cells induced by fumonisin B1 via TNF signalling pathway. Food and Chemical Toxicology 2020, 139, 111274 .

AMA Style

Jia Chen, Shuhua Yang, Sheng Huang, Rong Yan, Mingyang Wang, Si Chen, Jing Cai, Miao Long, Peng Li. Transcriptome study reveals apoptosis of porcine kidney cells induced by fumonisin B1 via TNF signalling pathway. Food and Chemical Toxicology. 2020; 139 ():111274.

Chicago/Turabian Style

Jia Chen; Shuhua Yang; Sheng Huang; Rong Yan; Mingyang Wang; Si Chen; Jing Cai; Miao Long; Peng Li. 2020. "Transcriptome study reveals apoptosis of porcine kidney cells induced by fumonisin B1 via TNF signalling pathway." Food and Chemical Toxicology 139, no. : 111274.

Journal article
Published: 18 March 2020 in Molecules
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The present study aimed to investigate the effects of astaxanthin (ASX) on ochratoxin A (OTA)-induced renal oxidative stress and its mechanism of action. Serum kidney markers, histomorphology, ultrastructural observation, and oxidative stress indicators were assessed. Meanwhile, quantitative real-time reverse transcription PCR and western blotting detection of NRF2 (encoding nuclear factor, erythroid 2 like) and members of the NRF2/KEAP1 signaling pathway (KEAP1 (encoding Kelch-like ECH-associated protein), NQO1 (encoding NAD(P)H quinone dehydrogenase), HO-1 (encoding heme oxygenase 1), γ-GCS (gamma-glutamylcysteine synthetase), and GSH-Px (glutathione peroxidase 1)) were performed. Compared with the control group, the OTA-treated group showed significantly increased levels of serum UA (uric acid) and BUN (blood urea nitrogen), tubular epithelial cells were swollen and degenerated, and the levels of antioxidant enzymes decreased significantly, and the expression of NRF2 (cytoplasm), NQO1, HO-1, γ-GCS, and GSH-Px decreased significantly. More importantly, after ASX pretreatment, compared with the OTA group, serum markers were decreased, epithelial cells appeared normal; the expression of antioxidant enzymes increased significantly, NQO1, HO-1, γ-GCS and GSH-Px levels increased significantly, and ASX promoted the transfer of NRF2 from the cytoplasm to the nucleus. These results highlight the protective ability of ASX in renal injury caused by OTA exposure, and provide theoretical support for ASX’s role in other mycotoxin-induced damage.

ACS Style

Lin Li; Yueli Chen; Danyang Jiao; Shuhua Yang; Peng Li; Lin Li. Protective Effect of Astaxanthin on Ochratoxin A-Induced Kidney Injury to Mice by Regulating Oxidative Stress-Related NRF2/KEAP1 Pathway. Molecules 2020, 25, 1386 .

AMA Style

Lin Li, Yueli Chen, Danyang Jiao, Shuhua Yang, Peng Li, Lin Li. Protective Effect of Astaxanthin on Ochratoxin A-Induced Kidney Injury to Mice by Regulating Oxidative Stress-Related NRF2/KEAP1 Pathway. Molecules. 2020; 25 (6):1386.

Chicago/Turabian Style

Lin Li; Yueli Chen; Danyang Jiao; Shuhua Yang; Peng Li; Lin Li. 2020. "Protective Effect of Astaxanthin on Ochratoxin A-Induced Kidney Injury to Mice by Regulating Oxidative Stress-Related NRF2/KEAP1 Pathway." Molecules 25, no. 6: 1386.

Research article
Published: 04 March 2020 in Oxidative Medicine and Cellular Longevity
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This study assessed the protective mechanism of astaxanthin (ASX) against ochratoxin A- (OTA-) induced cardiac injury in mice. Four groups of mice were established: control group (0.1 mL olive oil+0.1 mL NaHCO2), OTA group (0.1 mL OTA 5 mg/kg body weight), ASX group (0.1 mL ASX 100 mg/kg body weight), and ASX + OTA group (0.1 mL ASX 100 mg/kg body weight, 2 h later, 0.1 mL OTA 5 mg/kg body weight). The test period lasted for 27 days (7 days of dosing, 2 days of rest). Electrocardiogram, body weight, heart weight, tissue pathology, oxidative markers (malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH)), biochemical markers (creatine kinase (CK), creatine kinase isoenzyme (CK-MB), and lactate dehydrogenase (LDH)), electron microscopy, TUNEL, and Western blot tests were used to examine the effects of OTA on myocardial injury and ASX detoxification. The results showed that OTA exposure significantly decreased both body weight and heart weight. OTA induced a decrease in heart rate in mice and decreased tissue concentrations of SOD, CAT, and GSH, while increasing serum concentrations of cardiac enzymes (CK, CK-MB, and LDH) and tissue MDA. ASX improved heart rate, cardiac enzymes, and antioxidant levels in mice. The results of tissue pathology and TUNEL assay showed that ASX protects against OTA-induced myocardial injury. In addition, Western blot results showed that the OTA group upregulated Keap1, Bax, Caspase3, and Caspase9, while it downregulated Nrf2, HO-1, and Bcl-2 protein expression. ASX played a protective role by changing the expression of Keap1, Nrf2, HO-1, Bax, Bcl-2, Caspase3, and Caspase9 proteins. These results indicate that the protective mechanism of ASX on the myocardium works through the Keap1-Nrf2 signaling pathway and mitochondria-mediated apoptosis pathway. This study provides a molecular rationale for the mechanism underlying OTA-induced myocardial injury and the protective effect of ASX on the myocardium.

ACS Style

Gengyuan Cui; Lin Li; Weixiang Xu; Mingyang Wang; Danyang Jiao; Beibei Yao; Ketao Xu; Yueli Chen; Shuhua Yang; Miao Long; Peng Li; Yang Guo. Astaxanthin Protects Ochratoxin A-Induced Oxidative Stress and Apoptosis in the Heart via the Nrf2 Pathway. Oxidative Medicine and Cellular Longevity 2020, 2020, 1 -11.

AMA Style

Gengyuan Cui, Lin Li, Weixiang Xu, Mingyang Wang, Danyang Jiao, Beibei Yao, Ketao Xu, Yueli Chen, Shuhua Yang, Miao Long, Peng Li, Yang Guo. Astaxanthin Protects Ochratoxin A-Induced Oxidative Stress and Apoptosis in the Heart via the Nrf2 Pathway. Oxidative Medicine and Cellular Longevity. 2020; 2020 ():1-11.

Chicago/Turabian Style

Gengyuan Cui; Lin Li; Weixiang Xu; Mingyang Wang; Danyang Jiao; Beibei Yao; Ketao Xu; Yueli Chen; Shuhua Yang; Miao Long; Peng Li; Yang Guo. 2020. "Astaxanthin Protects Ochratoxin A-Induced Oxidative Stress and Apoptosis in the Heart via the Nrf2 Pathway." Oxidative Medicine and Cellular Longevity 2020, no. : 1-11.

Journal article
Published: 25 February 2020 in Toxins
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The aim of this study was to investigate the protective effects of selenium yeast (Se-Y) against hepatotoxicity induced by ochratoxin A (OTA). The OTA-induced liver injury model was established in chickens by daily oral gavage of 50 µg/kg OTA for 21 days. Serum biochemistry analysis, antioxidant analysis, as well as the qRT-PCR and Western blot (WB) analyses were then used to evaluate oxidative damage and apoptosis in chicken liver tissue. The results showed that Se-Y significantly increased liver coefficient induced by OTA (P < 0.05). OTA + Se-Y treated group revealed that Se-Y reduced the OTA-induced increase in glutamic pyruvic transaminase (ALT), glutamic oxaloacetic transaminase (AST) and malonaldehyde (MDA) content, and reversed the decrease in antioxidant capacity (T-AOC), glutathione peroxidase (GSH-Px) and total superoxide dismutase (T-SOD) (P < 0.05). In this study, we found that OTA is involved in the mRNA expression levels about Nrf2/Keap1 and PI3K/AKT signaling pathways, such as oxidative stress-related genes (Nrf2, GSH-Px, GLRX2 and Keap1) and apoptosis-related genes (Bax, Caspase3, P53, AKT, PI3K and Bcl-2). Besides, significant downregulations of protein expression of HO-1, MnSOD, Nrf2 and Bcl-2, as well as a significant upregulation of Caspase3 and Bax levels were observed after contaminated with OTA (P < 0.05). Notably, OTA-induced apoptosis and oxidative damage in the liver of chickens were reverted back to normal level in the OTA + Se-Y group. Our findings indicate that pretreatment with Se-Y effectively ameliorates OTA-induced hepatotoxicity.

ACS Style

Peng Li; Kang Li; Chao Zou; Cui Tong; Lin Sun; Zhongjun Cao; Shuhua Yang; Qiufeng Lyu. Selenium Yeast Alleviates Ochratoxin A-Induced Hepatotoxicity via Modulation of the PI3K/AKT and Nrf2/Keap1 Signaling Pathways in Chickens. Toxins 2020, 12, 143 .

AMA Style

Peng Li, Kang Li, Chao Zou, Cui Tong, Lin Sun, Zhongjun Cao, Shuhua Yang, Qiufeng Lyu. Selenium Yeast Alleviates Ochratoxin A-Induced Hepatotoxicity via Modulation of the PI3K/AKT and Nrf2/Keap1 Signaling Pathways in Chickens. Toxins. 2020; 12 (3):143.

Chicago/Turabian Style

Peng Li; Kang Li; Chao Zou; Cui Tong; Lin Sun; Zhongjun Cao; Shuhua Yang; Qiufeng Lyu. 2020. "Selenium Yeast Alleviates Ochratoxin A-Induced Hepatotoxicity via Modulation of the PI3K/AKT and Nrf2/Keap1 Signaling Pathways in Chickens." Toxins 12, no. 3: 143.

Research article
Published: 20 February 2020 in Oxidative Medicine and Cellular Longevity
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The purpose of this study was to investigate the protective effect and mechanism of yeast selenium (Se-Y) on ochratoxin- (OTA-) induced nephrotoxicity of chickens. A total of 80 one-day-old healthy chickens were randomly divided into 4 equal groups: control, OTA (50 μg/kg OTA), Se-Y (0.4 mg/kg Se-Y), and OTA+Se-Y (50 μg/kg OTA+0.4 mg/kg Se-Y). In the OTA chickens, differences in body weight, kidney coefficient, biochemical histological analysis, antioxidant capability, and the expression levels of the PI3K/AKT and Nrf2/Keap1 signaling pathway-related genes were observed. The levels of total superoxide dismutase (T-SOD), antioxidant capacity (T-AOC), catalase (CAT), and glutathione (T-GSH) significantly decreased, but the malondialdehyde (MDA) level of the kidneys significantly increased in the OTA treatment group. More importantly, treatment with Se-Y improved the antioxidant enzyme activities within the kidneys of chickens exposed to OTA. In addition, administration of OTA resulted in apoptosis and was associated with decreased expression of AKT, PI3K, and Bcl-2, which in turn enhanced expression of Caspase3, Bax, and P53. However, Se-Y improved the antioxidant defense system through activation of the Nrf2/Keap1 signaling pathway. Gene expression of Nrf2 and its target genes (HO-1, GSH-px, GLRX2, MnSOD, and CAT) was downregulated following OTA exposure. Conversely, Se-Y treatment resulted in a significant upregulation of the same genes. Besides, significant downregulations of protein expression of HO-1, CAT, MnSOD, Nrf2, and Bcl-2 and a significant upregulation of Caspase3 and Bax levels were observed after contaminated with OTA. Notably, OTA-induced apoptosis and oxidative damage in the kidney of chickens were reverted back to normal level in the OTA+Se-Y group. Taken together, the data suggest that Se-Y alleviates OTA-induced nephrotoxicity in chickens, possibly through the activation of the PI3K/AKT and Nrf2/Keap1 signaling pathways.

ACS Style

Kang Li; Zhongjun Cao; Yang Guo; Cui Tong; Shuhua Yang; Miao Long; Peng Li; Jianbin He. Selenium Yeast Alleviates Ochratoxin A-Induced Apoptosis and Oxidative Stress via Modulation of the PI3K/AKT and Nrf2/Keap1 Signaling Pathways in the Kidneys of Chickens. Oxidative Medicine and Cellular Longevity 2020, 2020, 4048706 -12.

AMA Style

Kang Li, Zhongjun Cao, Yang Guo, Cui Tong, Shuhua Yang, Miao Long, Peng Li, Jianbin He. Selenium Yeast Alleviates Ochratoxin A-Induced Apoptosis and Oxidative Stress via Modulation of the PI3K/AKT and Nrf2/Keap1 Signaling Pathways in the Kidneys of Chickens. Oxidative Medicine and Cellular Longevity. 2020; 2020 ():4048706-12.

Chicago/Turabian Style

Kang Li; Zhongjun Cao; Yang Guo; Cui Tong; Shuhua Yang; Miao Long; Peng Li; Jianbin He. 2020. "Selenium Yeast Alleviates Ochratoxin A-Induced Apoptosis and Oxidative Stress via Modulation of the PI3K/AKT and Nrf2/Keap1 Signaling Pathways in the Kidneys of Chickens." Oxidative Medicine and Cellular Longevity 2020, no. : 4048706-12.

Journal article
Published: 31 January 2020 in Journal of Functional Foods
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The aim was to investigate whether selenium-enriched yeast (SeY) can attenuate intestinal injury in broiler chickens induced by ochratoxin A (OTA). Here, the results showed that SeY addition increased the body weight, feed conversion ratio, villi height, villus/crypt ratio, and the numbers of goblet cells. Furthermore, the levels of oxidative stress by SeY addition (superoxide dismutase activity, total antioxidant capacity, and total glutathione content) were significantly decreased (P < 0.01), but the malondialdehyde content was significantly increased (P < 0.05). Moreover, nuclear transcription factor-κB (NF-κB), interleukin-1beta and tumor necrosis factor-α mRNA expressions were significantly decreased (P < 0.01) by SeY addition, but nuclear factor erythroid-2 related factor 2 (Nrf2) and heme oxygenase-1 were significantly increased (P < 0.05). In addition, western blotting results indicated that SeY normalized the OTA-induced phosphorylation of NF-κB and Nrf2. In summary, SeY alleviates OTA-induced intestinal toxicity in broiler chickens by activating the Nrf2 pathway and inhibiting NF-κB activation.

ACS Style

Cui Tong; Peng Li; Li-Hui Yu; Lin Li; Kang Li; Yueli Chen; Shu-Hua Yang; Miao Long. Selenium-rich yeast attenuates ochratoxin A-induced small intestinal injury in broiler chickens by activating the Nrf2 pathway and inhibiting NF-KB activation. Journal of Functional Foods 2020, 66, 103784 .

AMA Style

Cui Tong, Peng Li, Li-Hui Yu, Lin Li, Kang Li, Yueli Chen, Shu-Hua Yang, Miao Long. Selenium-rich yeast attenuates ochratoxin A-induced small intestinal injury in broiler chickens by activating the Nrf2 pathway and inhibiting NF-KB activation. Journal of Functional Foods. 2020; 66 ():103784.

Chicago/Turabian Style

Cui Tong; Peng Li; Li-Hui Yu; Lin Li; Kang Li; Yueli Chen; Shu-Hua Yang; Miao Long. 2020. "Selenium-rich yeast attenuates ochratoxin A-induced small intestinal injury in broiler chickens by activating the Nrf2 pathway and inhibiting NF-KB activation." Journal of Functional Foods 66, no. : 103784.

Journal article
Published: 23 January 2020 in Food and Chemical Toxicology
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We investigated the protective effect and mechanism of selenium-enriched yeast (SY) on caecal injury induced by ochratoxin A (OTA) in broilers. Eighty broiler chickens of 1-day-old with similar weight were randomly assigned to Control group, OTA group, SY group and OTA + SY group, and were intragastricaly administered with OTA and SY for 21 consecutive days. The results showed that SY could reduce the caecal pathological injuries and could inhibit oxidative stress caused by OTA exposure. The OTA + SY group showed a statistically significant (p < 0.01) reduction in the level of MDA, IL-1β, IL-6 and IFN-γ, whereas the levels of GSH, SOD activity and IL-10 were significantly increased (p < 0.01). By regulating TLR4/MYD88 signaling pathway, SY inhibited the expression of NF-κB, increased the expression of tight junction-related genes Claudin-1, Occludin and ZO-1, and antagonized the intestinal barrier injury caused by OTA exposure. Moreover, the microbial diversity analyses indicated that SY could intervene changes in the diversity of gut microbiota and the imbalance of gut microbiota caused by OTA. SY could relieve caecal pathological injuries, alleviate OTA-induced caecal oxidative stress and inflammatory response, increase the gut microbial diversity and protect broiler's intestinal barrier from injury.

ACS Style

Shuhua Yang; Lin Li; Lihui Yu; Lin Sun; Kang Li; Cui Tong; Weixiang Xu; Gengyuan Cui; Miao Long; Peng Li. Selenium-enriched yeast reduces caecal pathological injuries and intervenes changes of the diversity of caecal microbiota caused by Ochratoxin-A in broilers. Food and Chemical Toxicology 2020, 137, 111139 .

AMA Style

Shuhua Yang, Lin Li, Lihui Yu, Lin Sun, Kang Li, Cui Tong, Weixiang Xu, Gengyuan Cui, Miao Long, Peng Li. Selenium-enriched yeast reduces caecal pathological injuries and intervenes changes of the diversity of caecal microbiota caused by Ochratoxin-A in broilers. Food and Chemical Toxicology. 2020; 137 ():111139.

Chicago/Turabian Style

Shuhua Yang; Lin Li; Lihui Yu; Lin Sun; Kang Li; Cui Tong; Weixiang Xu; Gengyuan Cui; Miao Long; Peng Li. 2020. "Selenium-enriched yeast reduces caecal pathological injuries and intervenes changes of the diversity of caecal microbiota caused by Ochratoxin-A in broilers." Food and Chemical Toxicology 137, no. : 111139.

Journal article
Published: 17 September 2019 in Toxins
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The aim of this research was to evaluate the potential protective mechanism of astaxanthin (ASTA) against oxidative damage and inflammation caused by ochratoxin (OTA) in mouse lung. We divided mice into a control group (CG), an OTA group (PG), an astaxanthin group (AG), and an OTA+ASTA group (JG). Oxidative indices (malondialdehyde (MDA), total superoxide dismutase (T-SOD), and reduced glutathione (GSH)) and inflammatory markers (interleukin 1β (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α)) were assayed in the lung, and the lung-weight-to-body-weight ratio was calculated. Apoptosis was detected in pathological sections by the TdT-mediated dUTP nick-end labeling (TUNEL) assay. Oxidative damage and inflammation were detected in the lung of mice after exposure to OTA. Besides, Nrf2- and NF-κB-pathway-associated proteins were detected by Western blot. In contrast with OTA, ASTA significantly raised the expression of Nrf2, HO-1, and MnSOD, while the expression of other proteins (Keap1, TLR4, and NF-κB) was significantly decreased. These results indicate that ASTA exerted protective effects against OTA-induced oxidative damage and inflammation in the lung by regulating the Nrf2 and NF-κB pathways.

ACS Style

Weixiang Xu; Mingyang Wang; Gengyuan Cui; Lin Li; Danyang Jiao; Beibei Yao; Ketao Xu; Yueli Chen; Miao Long; Shuhua Yang; Jianbin He. Astaxanthin Protects OTA-Induced Lung Injury in Mice through the Nrf2/NF-κB Pathway. Toxins 2019, 11, 540 .

AMA Style

Weixiang Xu, Mingyang Wang, Gengyuan Cui, Lin Li, Danyang Jiao, Beibei Yao, Ketao Xu, Yueli Chen, Miao Long, Shuhua Yang, Jianbin He. Astaxanthin Protects OTA-Induced Lung Injury in Mice through the Nrf2/NF-κB Pathway. Toxins. 2019; 11 (9):540.

Chicago/Turabian Style

Weixiang Xu; Mingyang Wang; Gengyuan Cui; Lin Li; Danyang Jiao; Beibei Yao; Ketao Xu; Yueli Chen; Miao Long; Shuhua Yang; Jianbin He. 2019. "Astaxanthin Protects OTA-Induced Lung Injury in Mice through the Nrf2/NF-κB Pathway." Toxins 11, no. 9: 540.

Journal article
Published: 16 August 2019 in Microorganisms
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Zearalenone (ZEA) contamination is a very serious problem around the world as it can induce reproductive disorders in animals and affect the health of humans. Therefore, reducing the damage it causes to humans and animals is a current focus of research. In this study, we assess the removing capacity of Pediococcus pentosaceus xy46 towards ZEA and investigate the mechanism responsible for its action, thus confirming if it can alleviate ZEA toxicity to the reproductive systems of male mice. Our results show that the rate at which the strain removes ZEA is as high as 89.2% in 48 h when the concentration of ZEA is 4 μg/mL in the liquid medium. Heat and acid treatment significantly enhanced the ability of the bacteria to remove ZEA. The animal experiments results show that the oral administration of xy46 to mice (0.2 mL daily at a concentration of 109 CFU/mL for 28 days) significantly reduces the degree of testicular pathomorphological changes and apoptosis induced by ZEA when the mice are intragastric administration with 40 mg/kg ZEA daily for 28 days. Moreover, oral administration of xy46 enhances the decrease in the testosterone level and improves the oxidative stress injury induced by ZEA. Furthermore, oral administration of xy46 reverts the expression of these genes and proteins in the testicular tissues of the mice involved in the blood–testis barrier and apoptosis (e.g., Vim, caspase 12, Cldn11, N-cad, Bax, and Bcl-2). However, xy46 cannot significantly revert in some of these evaluated parameters, especially in sperm quantity and quality when the mice were given 70 mg/kg ZEA daily for 28 days. In conclusion, our results suggest that the strain Pediococcus pentosaceus xy46 can efficiently remove ZEA from the liquid medium, the mechanism responsible for its action is absorption, and it can alleviate the toxicity of ZEA to the reproductive systems of male mice when the mice are given 40 mg/kg ZEA daily, However, it cannot completely alleviate the reproductive toxicity of higher dosage of zearalenone through its ability to adsorb ZEA.

ACS Style

Shuhua Yang; Ping Gong; Jianwen Pan; Wang; Jingjing Tong; Miao Long; Peng Li; Jianbin He; Yang; Gong; Pan; Tong; Long; Li; He; Nan Wang; Mingyang Wang. Pediococcus pentosaceus xy46 Can Absorb Zearalenone and Alleviate its Toxicity to the Reproductive Systems of Male Mice. Microorganisms 2019, 7, 266 .

AMA Style

Shuhua Yang, Ping Gong, Jianwen Pan, Wang, Jingjing Tong, Miao Long, Peng Li, Jianbin He, Yang, Gong, Pan, Tong, Long, Li, He, Nan Wang, Mingyang Wang. Pediococcus pentosaceus xy46 Can Absorb Zearalenone and Alleviate its Toxicity to the Reproductive Systems of Male Mice. Microorganisms. 2019; 7 (8):266.

Chicago/Turabian Style

Shuhua Yang; Ping Gong; Jianwen Pan; Wang; Jingjing Tong; Miao Long; Peng Li; Jianbin He; Yang; Gong; Pan; Tong; Long; Li; He; Nan Wang; Mingyang Wang. 2019. "Pediococcus pentosaceus xy46 Can Absorb Zearalenone and Alleviate its Toxicity to the Reproductive Systems of Male Mice." Microorganisms 7, no. 8: 266.

Journal article
Published: 01 February 2019 in International Journal of Molecular Sciences
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Zearalenone (ZEN), an important environmental pollutant, can cause serious harm to human and animal health. The aim of our study was to examine the effect of zearalenone (ZEN) on miRNA expression profiles in the mouse Leydig cell line (TM3 Leydig cell line) by miRNA sequencing. The effect of ZEN on the viability of TM3 Leydig cells was verified by Cell Counting Kit-8 (CCK-8). MiRNA sequencing was performed 24 h after the exposure of TM3 Leydig cells with 50 μmol/L of ZEN. Bioinformatics predicted the miRNA target genes, performed Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, and conducted miRNA-gene-pathway mapping to show the relationship between miRNA, the target gene, and the signalling pathway. The expression levels of miRNA and the miRNA target genes associated with ZEN toxicology were verified by quantitative real-time polymerase chain reaction. The miRNA sequencing revealed a significant change (p < 0.05) in the 197 miRNAs in the ZEN-treated and control groups, among which 86 were up-regulated and 111 were down-regulated. GO analysis of the target genes of these miRNAs indicated various biological functions. KEGG analysis showed that the predicted miRNA target genes were involved in signalling pathways, such as cancer, apoptosis, and oxidation, namely, the Ras signalling pathway, Rap1 signalling pathway, PI3K-AKT signalling pathway, Foxo signalling pathway, and AMPK signalling pathway. These results suggest that ZEN, as an estrogen-like toxin, is regulated by microRNAs. Our results can help to examine the toxicological effects of ZEN-regulated miRNAs on germ cells.

ACS Style

Mingyang Wang; Weiwei Wu; Lin Li; Jianbin He; Sheng Huang; Si Chen; Jia Chen; Miao Long; Shuhua Yang; Peng Li. Analysis of the miRNA Expression Profiles in the Zearalenone-Exposed TM3 Leydig Cell Line. International Journal of Molecular Sciences 2019, 20, 635 .

AMA Style

Mingyang Wang, Weiwei Wu, Lin Li, Jianbin He, Sheng Huang, Si Chen, Jia Chen, Miao Long, Shuhua Yang, Peng Li. Analysis of the miRNA Expression Profiles in the Zearalenone-Exposed TM3 Leydig Cell Line. International Journal of Molecular Sciences. 2019; 20 (3):635.

Chicago/Turabian Style

Mingyang Wang; Weiwei Wu; Lin Li; Jianbin He; Sheng Huang; Si Chen; Jia Chen; Miao Long; Shuhua Yang; Peng Li. 2019. "Analysis of the miRNA Expression Profiles in the Zearalenone-Exposed TM3 Leydig Cell Line." International Journal of Molecular Sciences 20, no. 3: 635.

Journal article
Published: 01 February 2019 in International Journal of Molecular Sciences
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Cadmium (Cd) is harmful for humans and animals, especially for the reproductive system. However, the mechanism of its toxicity has not been elucidated, and how to alleviate its toxicity is very important. This study aimed to explore the role and mechanism of action of sulforaphane (SFN) in protecting mouse Leydigs (TM3) cells from cadmium (Cd)-induced damage. The half-maximal inhibitory concentration (IC50) of Cd and the safe doses of SFN were determined using a methyl thiazolyl tetrazolium (MTT) assay. The testosterone secretion from TM3 cells was measured using the enzyme-linked immunosorbent assay. The intracellular oxidative stress was evaluated using corresponding kits. The cell apoptosis was detected using flow cytometry. The mRNA expression of genes associated with NF-E2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling was detected using reverse transcription–polymerase chain reaction, including Nrf2, heme oxygenase I (HO-1), glutathione peroxidase (GSH-Px), NAD(P)H:quinone acceptor oxidoreductase 1 (NQO1), and γ-glutamylcysteine synthetase (γ-GCS). The protein expression of Nrf2, GSH-Px, HO-1, γ-GCS, and NQO1 was detected using Western blot analysis. The results showed that the IC50 of Cd to TM3 cells was 51.4 µmol/L. SFN reduced the release of lactate dehydrogenase from Cd-exposed cells. Cd + SFN 2.5 treatment significantly elevated testosterone concentration compared with the Cd group (p < 0.05). SFN significantly increased total superoxide dismutase (T-SOD) and GSH-Px activity and GSH content in Cd-treated cells (p < 0.05; p < 0.01), inhibited the production of malondialdehyde or reactive oxygen species caused by Cd (p < 0.05; p < 0.01), and reduced the apoptotic rate of Cd-induced TM3 cells (p < 0.01). SFN upregulated the mRNA expression of Nrf2, GSH-Px, HO-1, NQO1, and γ-GCS in Cd-treated cells, indicating the protective effect of SFN against Cd-induced oxidative stress or cell apoptosis by activating the Nrf2/ARE signaling pathway.

ACS Style

Shu-Hua Yang; Peng Li; Li-Hui Yu; Lin Li; Miao Long; Ming-Da Liu; Jian-Bin He. Sulforaphane Protect Against Cadmium-Induced Oxidative Damage in mouse Leydigs cells by Activating Nrf2/ARE Signaling Pathway. International Journal of Molecular Sciences 2019, 20, 630 .

AMA Style

Shu-Hua Yang, Peng Li, Li-Hui Yu, Lin Li, Miao Long, Ming-Da Liu, Jian-Bin He. Sulforaphane Protect Against Cadmium-Induced Oxidative Damage in mouse Leydigs cells by Activating Nrf2/ARE Signaling Pathway. International Journal of Molecular Sciences. 2019; 20 (3):630.

Chicago/Turabian Style

Shu-Hua Yang; Peng Li; Li-Hui Yu; Lin Li; Miao Long; Ming-Da Liu; Jian-Bin He. 2019. "Sulforaphane Protect Against Cadmium-Induced Oxidative Damage in mouse Leydigs cells by Activating Nrf2/ARE Signaling Pathway." International Journal of Molecular Sciences 20, no. 3: 630.

Journal article
Published: 31 October 2018 in Toxins
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Zearalenone (ZEN) is an estrogen-like mycotoxin produced by Fusarium that seriously compromises the safety of animal and human health. In this study, our aim was to evaluate the protective effect of Bacillus velezensis A2 against biochemical and pathological changes induced by zearalenone in mice. Kunming mice (n = 40; 25 ± 2 g) were allotted to four treatment groups: a control group (basic feed); a ZEN group (basic feed with a ZEN dose of 60 mg/kg); an A2 strain fermented feed group (150 g of feed mixed with 150 mL of sterile distilled water and inoculated with 5 mL of phosphate buffer salt (PBS) resuspended A2 strain); and an A2 strain fermented ZEN-contaminated feed group. (A2 strain group 150 mL pure bacterial distilled water system mixed with 150 g ZEN-contaminated feed.) Our results showed that the Bacillus velezensis A2 strain can completely degrade the ZEN-contaminated feed within 5 days. (The concentration of ZEN in fermentation was 60 μg/mL.) After the mice fed for 28 days, compared with the control group, the activities of AST and ALT were increased, the activities of glutathione peroxidase (GSH-PX) and total superoxide dismutase (T-SOD) were decreased, and the amount of creatinine (CRE), blood urea nitrogen (BUN), uric acid (UA), and malondialdehyde (MDA) in the ZEN group were increased in the mice serum (p < 0.05; p < 0.01). However, compared with the ZEN group, these biochemical levels were reversed in the A2 strain fermented feed group and in the A2 strain fermented ZEN-contaminated feed group (p < 0.05; p < 0.01). Furthermore, histopathological analysis only showed pathological changes of the mice liver in the ZEN group. The results showed that Bacillus velezensis A2 as additive could effectively remove ZEN contamination in the feed and protect the mice against the toxic damage of ZEN. In conclusion, Bacillus velezensis A2 has great potential use as a microbial feed additive to detoxify the toxicity of zearalenone in production practice.

ACS Style

Nan Wang; Peng Li; Mingyang Wang; Si Chen; Sheng Huang; Miao Long; Shuhua Yang; Jianbin He. The Protective Role of Bacillus velezensis A2 on the Biochemical and Hepatic Toxicity of Zearalenone in Mice. Toxins 2018, 10, 449 .

AMA Style

Nan Wang, Peng Li, Mingyang Wang, Si Chen, Sheng Huang, Miao Long, Shuhua Yang, Jianbin He. The Protective Role of Bacillus velezensis A2 on the Biochemical and Hepatic Toxicity of Zearalenone in Mice. Toxins. 2018; 10 (11):449.

Chicago/Turabian Style

Nan Wang; Peng Li; Mingyang Wang; Si Chen; Sheng Huang; Miao Long; Shuhua Yang; Jianbin He. 2018. "The Protective Role of Bacillus velezensis A2 on the Biochemical and Hepatic Toxicity of Zearalenone in Mice." Toxins 10, no. 11: 449.

Journal article
Published: 11 September 2018 in Scientific Reports
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Zearalenone (ZEN) is an estrogen-like mycotoxin occurring in food and feeds, and it can cause oxidative damage and apoptosis in the testis, liver, and kidney. A current concern for researchers is how to reduce the harm it causes to humans and animals. In this study, our aim was to isolate and identify a novel and efficient ZEN-detoxifying strain of bacteria, and we aimed to assess the protective effect of the isolated strain on kidney damage caused by ZEN in mice. Our results indicated that a strain of Bacillus velezensis (B. velezensis), named A2, could completely degrade ZEN (7.45 μg/mL) after three days of incubation at 37 °C in the Luria-Bertani (LB) medium. This fermentation broth of the B. velezensis A2 strain was given to mice. The histopathological analysis indicated that the fermentation broth from the B. velezensis A2 strain reduced the degree of renal injury that is induced by ZEN. Furthermore, it greatly reduced the increase in serum levels of creatinine (CRE), uric acid (UA), and urea nitrogen (BUN) caused by ZEN. In addition, B. velezensis A2 strain also significantly inhibited the increase of malonaldehyde (MDA) content, and reversed the decreases of total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-Px) activities caused by ZEN. Studies have shown that ZEN is involved in the regulation of mRNA and protein levels of genes involved in the ER stress-induced apoptotic pathway, such as heavy chain binding protein (BIP), C-/-EBP homologous protein (CHOP), cysteine Aspartate-specific protease-12 (Caspase-12), c-Jun N-terminal kinase (JNK), and BCL2-related X protein (Bcl-2 and Bax). However, when mice were administered the fermentation broth of the B. velezensis A2 strain, it significantly reversed the expressions of these genes in their kidney tissue. In conclusion, our results indicate that the newly identified strain of B. velezensis A2, has a protective effect from renal injury induced by ZEN in mice. This strain has a potential application in the detoxification of ZEN in feed and protects animals from ZEN poisoning.

ACS Style

Nan Wang; Peng Li; Jiawen Pan; Mingyang Wang; Miao Long; Jian Zang; Shuhua Yang. Bacillus velezensis A2 fermentation exerts a protective effect on renal injury induced by Zearalenone in mice. Scientific Reports 2018, 8, 1 -14.

AMA Style

Nan Wang, Peng Li, Jiawen Pan, Mingyang Wang, Miao Long, Jian Zang, Shuhua Yang. Bacillus velezensis A2 fermentation exerts a protective effect on renal injury induced by Zearalenone in mice. Scientific Reports. 2018; 8 (1):1-14.

Chicago/Turabian Style

Nan Wang; Peng Li; Jiawen Pan; Mingyang Wang; Miao Long; Jian Zang; Shuhua Yang. 2018. "Bacillus velezensis A2 fermentation exerts a protective effect on renal injury induced by Zearalenone in mice." Scientific Reports 8, no. 1: 1-14.

Journal article
Published: 19 July 2018 in Molecules
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The present study evaluated the mechanism underlying the protective effect of sulforaphane (SFN) on cadmium (Cd)-induced Sertoli cell (TM4 cells) injury in mice. The apoptosis rate of cells in each group was detected by flow cytometry. It was determined the effect of SFN on the expression of downstream molecular targets of Nrf2/ARE axis and on the lipid peroxide content. The related genes involved in the nuclear factor E2-related factor 2(Nrf2)/antioxidant response element (ARE) signaling pathway were evaluated by RT-PCR; for example, the mRNA expression levels of Nrf2, heme oxygenase-1 (HO-1), glutathione peroxidase (GSH-Px), quinone oxidoreductase 1 (NQO1), and γ-glutamylcysteine synthetase (γ-GCS), while the protein expression levels were assessed by Western blot. Our results showed that the mRNA and protein expression levels of Nrf2, HO-1, NQO1, GSH-Px, and γ-GCS were increased in various degree when the Sertoli cells were to added different concentrations of SFN. Our results also showed that SFN reduced the apoptosis rate, increased the activity of T-SOD, inhibited the increase of the MDA content caused by Cd. Meanwhile, SFN could increase the mRNA and protein expression levels of Nrf2, HO-1 and NQO1 and reduced the mRNA and protein expression levels of GSH-Px and γ-GCS caused by Cd in Sertoli cells (p < 0.01). Taken together, SFN could improve the antioxidant capacity of Sertoli cells, and exert a protective effect on the oxidative damage and apoptosis of Cd-induced Sertoli cells through the activation of Nrf2/ARE signal transduction pathway.

ACS Style

Shu-Hua Yang; Li-Hui Yu; Lin Li; Yang Guo; Yi Zhang; Miao Long; Peng Li; Jian-Bin He. Protective Mechanism of Sulforaphane on Cadmium-Induced Sertoli Cell Injury in Mice Testis via Nrf2/ARE Signaling Pathway. Molecules 2018, 23, 1774 .

AMA Style

Shu-Hua Yang, Li-Hui Yu, Lin Li, Yang Guo, Yi Zhang, Miao Long, Peng Li, Jian-Bin He. Protective Mechanism of Sulforaphane on Cadmium-Induced Sertoli Cell Injury in Mice Testis via Nrf2/ARE Signaling Pathway. Molecules. 2018; 23 (7):1774.

Chicago/Turabian Style

Shu-Hua Yang; Li-Hui Yu; Lin Li; Yang Guo; Yi Zhang; Miao Long; Peng Li; Jian-Bin He. 2018. "Protective Mechanism of Sulforaphane on Cadmium-Induced Sertoli Cell Injury in Mice Testis via Nrf2/ARE Signaling Pathway." Molecules 23, no. 7: 1774.