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JinJie Wu
College of Animal Science and Technology, Hefei, China

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Research article
Published: 22 June 2021 in Environmental Science and Pollution Research
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Zearalenone (ZEA) and Deoxynivalenol (DON) are two mycotoxins highly detected in agricultural products and feed. Both mycotoxins produce reproductive toxicity and pose a serious threat to human and animal health, among which pigs are the most sensitive animals. Sertoli cells (SCs) play an important role in spermatogenesis; however, the combined toxicity of ZEA and DON and the screening of effective protective agents remains to be determined. By studying the effects of N-acetylcysteine (NAC) on the cells exposed to 20 μM of ZEA and 0.6 μM of DON, we explored the protective mechanism of NAC (4 mM) on the cytotoxic injury of piglets SCs induced by both mycotoxins. The results showed that the combination of ZEA and DON destroy organelles and SCs structures, NAC significantly alleviates the damage caused by ZEA and DON. NAC also significantly increased the expression and distribution of zonula occludens 1 (ZO-1), decreased the relative mRNA and protein expression levels of Bax, Bid, caspase-3, and caspase-9, and increased Bcl-2 expression level and inhibited the decrease of mitochondrial membrane potential. Further, NAC also eases the cell cycle arrest and oxidative stress caused by ZEA and DON. In summary, our results show that NAC could alleviate SCs injury via reducing the oxidative damage and apoptosis caused by ZEA and DON.

ACS Style

Li Cao; Jie Zhao; Jingru Xu; Lei Zhu; Sajid Ur Rahman; Shibin Feng; Yu Li; JinJie Wu; Xichun Wang. N-acetylcysteine ameliorate cytotoxic injury in piglets sertoli cells induced by zearalenone and deoxynivalenol. Environmental Science and Pollution Research 2021, 1 -14.

AMA Style

Li Cao, Jie Zhao, Jingru Xu, Lei Zhu, Sajid Ur Rahman, Shibin Feng, Yu Li, JinJie Wu, Xichun Wang. N-acetylcysteine ameliorate cytotoxic injury in piglets sertoli cells induced by zearalenone and deoxynivalenol. Environmental Science and Pollution Research. 2021; ():1-14.

Chicago/Turabian Style

Li Cao; Jie Zhao; Jingru Xu; Lei Zhu; Sajid Ur Rahman; Shibin Feng; Yu Li; JinJie Wu; Xichun Wang. 2021. "N-acetylcysteine ameliorate cytotoxic injury in piglets sertoli cells induced by zearalenone and deoxynivalenol." Environmental Science and Pollution Research , no. : 1-14.

Journal article
Published: 01 April 2021 in Animal Bioscience
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Objective: Glucose transporter 9 (GLUT9) is a uric acid transporter that is associated with uric absorption in mice and humans; but it is unknown whether GLUT9 involves in chicken uric acid regulation. This experiment aimed to investigate the chicken GLUT9 expression and serum uric acid (SUA) level.Methods: Sixty chickens were divided into 4 groups (n = 15): a control group (NC); a sulfonamide-treated group (SD) supplemented with sulfamonomethoxine sodium via drinking water (8 mg/L); a fishmeal group (FM) supplemented with 16% fishmeal in diet; and a uric acid-injection group (IU), where uric acid (250 mg/kg) was intraperitoneally injected once a day. The serum was collected weekly to detect the SUA level. Liver, kidney, jejunum, and ileum tissues were collected to detect the GLUT9 mRNA and protein expression.Results: The results showed in the SD and IU groups, the SUA level increased and GLUT9 expression increased in the liver, but decreased in the kidney, jejunum, and ileum. In the FM group, the SUA level decreased slightly and GLUT9 expression increased in the kidney, but decreased in the liver, jejunum, and ileum. Correlation analysis revealed that liver GLUT9 expression correlated positively, and renal GLUT9 expression correlated negatively with the SUA level.Conclusion: These results demonstrate that there may be a feedback regulation of GLUT9 in the chicken liver and kidney to maintain the SUA balance; however, the underlying mechanism needs to be investigated in future studies.

ACS Style

Xuedong Ding; Chenglu Peng; Siting Li; Manman Li; Xinlu Li; Zhi Wang; Yu Li; Xichun Wang; Jinchun Li; Jinjie Wu Wu. Chicken serum uric acid level is regulated by glucose transporter 9. Animal Bioscience 2021, 34, 670 -679.

AMA Style

Xuedong Ding, Chenglu Peng, Siting Li, Manman Li, Xinlu Li, Zhi Wang, Yu Li, Xichun Wang, Jinchun Li, Jinjie Wu Wu. Chicken serum uric acid level is regulated by glucose transporter 9. Animal Bioscience. 2021; 34 (4):670-679.

Chicago/Turabian Style

Xuedong Ding; Chenglu Peng; Siting Li; Manman Li; Xinlu Li; Zhi Wang; Yu Li; Xichun Wang; Jinchun Li; Jinjie Wu Wu. 2021. "Chicken serum uric acid level is regulated by glucose transporter 9." Animal Bioscience 34, no. 4: 670-679.

Journal article
Published: 20 January 2021 in Toxins
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Deoxynivalenol (DON) is a common trichothecene mycotoxin found worldwide. DON has broad toxicity towards animals and humans. However, the mechanism of DON-induced neurotoxicity in vitro has not been fully understood. This study investigated the hypothesis that DON toxicity in neurons occurs via the mitochondrial apoptotic pathway. Using piglet hippocampal nerve cells (PHNCs), we evaluated the effects of different concentrations of DON on typical indicators of apoptosis. The obtained results demonstrated that DON treatment inhibited PHNC proliferation and led to morphological, biochemical, and transcriptional changes consistent with apoptosis, including decreased mitochondrial membrane potential, mitochondrial release of cytochrome C (CYCS) and apoptosis inducing factor (AIF), and increased abundance of active cleaved-caspase-9 and cleaved-caspase-3. Increasing concentrations of DON led to decreased B-cell lymphoma-2 (Bcl-2) expression and increased expression of BCL2-associated X (Bax) and B-cell lymphoma-2 homology 3 interacting domain death agonist (Bid), which in turn increased transcriptional activity of the transcription factors AIF and P53 (a tumor suppressor gene, promotes apoptosis). The addition of a caspase-8 inhibitor abrogated these effects. These results reveal that DON induces apoptosis in PHNCs via the mitochondrial apoptosis pathway, and caspase-8 is shown to play an important role during apoptosis regulation.

ACS Style

Li Cao; Yunjing Jiang; Lei Zhu; Wei Xu; Xiaoyan Chu; Yafei Zhang; Sajid Rahman; Shibin Feng; Yu Li; JinJie Wu; Xichun Wang. Deoxynivalenol Induces Caspase-8-Mediated Apoptosis through the Mitochondrial Pathway in Hippocampal Nerve Cells of Piglet. Toxins 2021, 13, 73 .

AMA Style

Li Cao, Yunjing Jiang, Lei Zhu, Wei Xu, Xiaoyan Chu, Yafei Zhang, Sajid Rahman, Shibin Feng, Yu Li, JinJie Wu, Xichun Wang. Deoxynivalenol Induces Caspase-8-Mediated Apoptosis through the Mitochondrial Pathway in Hippocampal Nerve Cells of Piglet. Toxins. 2021; 13 (2):73.

Chicago/Turabian Style

Li Cao; Yunjing Jiang; Lei Zhu; Wei Xu; Xiaoyan Chu; Yafei Zhang; Sajid Rahman; Shibin Feng; Yu Li; JinJie Wu; Xichun Wang. 2021. "Deoxynivalenol Induces Caspase-8-Mediated Apoptosis through the Mitochondrial Pathway in Hippocampal Nerve Cells of Piglet." Toxins 13, no. 2: 73.

Original research article
Published: 22 June 2020 in Journal of Cellular Physiology
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Epigallocatechin‐3‐gallate (EGCG) plays a crucial role in hepatic lipid metabolism. However, the underlying regulatory mechanism of hepatic lipid metabolism by EGCG in canine is unclear. Primary canine hepatocytes were treated with EGCG (0.01, 0.1, or 1 μM) and BML‐275 (an AMP‐activated protein kinase [AMPK] inhibitor) to study the effects of EGCG on the gene and protein expressions associated with AMPK signaling pathway. Data showed that treatment with EGCG had greater activation of AMPK, as well as greater expression levels and transcriptional activity of peroxisome proliferator activated receptor‐α (PPARα) along with upregulated messenger RNA (mRNA) abundance and protein abundance of PPARα‐target genes. EGCG decreased the expression levels and transcriptional activity of sterol regulatory element‐binding protein 1c (SREBP‐1c) along with downregulated mRNA abundance and protein abundance of SREBP‐1c target genes. Of particular interest, exogenous BML‐275 could reduce or eliminate the effects of EGCG on lipid metabolism in canine hepatocytes. Furthermore, the content of triglyceride was significantly decreased in the EGCG‐treated groups. These results suggest that EGCG might be a potential agent in preventing high‐fat diet‐induced lipid accumulation in small animals.

ACS Style

Hongyan Ding; Yu Li; Wei Li; Huanqing Tao; Leihong Liu; Cai Zhang; Tao Kong; Shibin Feng; Jinchun Li; Xichun Wang; JinJie Wu. Epigallocatechin‐3‐gallate activates the AMP‐activated protein kinase signaling pathway to reduce lipid accumulation in canine hepatocytes. Journal of Cellular Physiology 2020, 236, 405 -416.

AMA Style

Hongyan Ding, Yu Li, Wei Li, Huanqing Tao, Leihong Liu, Cai Zhang, Tao Kong, Shibin Feng, Jinchun Li, Xichun Wang, JinJie Wu. Epigallocatechin‐3‐gallate activates the AMP‐activated protein kinase signaling pathway to reduce lipid accumulation in canine hepatocytes. Journal of Cellular Physiology. 2020; 236 (1):405-416.

Chicago/Turabian Style

Hongyan Ding; Yu Li; Wei Li; Huanqing Tao; Leihong Liu; Cai Zhang; Tao Kong; Shibin Feng; Jinchun Li; Xichun Wang; JinJie Wu. 2020. "Epigallocatechin‐3‐gallate activates the AMP‐activated protein kinase signaling pathway to reduce lipid accumulation in canine hepatocytes." Journal of Cellular Physiology 236, no. 1: 405-416.

Preprint content
Published: 13 May 2020
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Background: Glycinin, a protein found in soybean, is a human and animal allergen that causes damage to the intestinal barrier. However, its mechanisms of action remain unclear. Therefore, in this study, the intestinal porcine epithelial cell line IPEC-J2 was used to evaluate the effect of glycinin concentration on the intestinal epithelium and identify the related signaling pathways. Results: IPEC-J2 cells were divided into seven treatment groups and a control group; the cells were treated for 24 h with 1, 5, or 10 mg/mL glycinin or with 5 mg/mL glycinin after 30 min of pre-treatment with 1 μmol/L nuclear factor-kappa B (NF-κB) inhibitor (pyrrolidine dithiocarbamate), inducible nitric oxide synthase inhibitor ( N -ω-nitro-l-arginine methyl ester), Jun N-terminal kinase (JNK) inhibitor (SP600125), or p38 inhibitor (SB202190). A series of molecular and biochemical experiments revealed that the levels of NF-κB, p38, and JNK, as well as their downstream proteins, were increased after treatment compared to those in the control group. Conclusion: Glycinin damaged IPEC-J2 cells in a concentration-dependent manner via the NF-κB/MAPK signaling pathway.

ACS Style

Chenglu Peng; Zhifeng Sun; Lei Wang; Yingshuang Shu; Mengchu He; Hongyan Ding; Yu Li; Xichun Wang; Shibin Feng; Jinchun Li; JinJie Wu. Glycinin-induced porcine IPEC-J2 cells damage via the NF-κB/MAPK signaling pathway. 2020, 1 .

AMA Style

Chenglu Peng, Zhifeng Sun, Lei Wang, Yingshuang Shu, Mengchu He, Hongyan Ding, Yu Li, Xichun Wang, Shibin Feng, Jinchun Li, JinJie Wu. Glycinin-induced porcine IPEC-J2 cells damage via the NF-κB/MAPK signaling pathway. . 2020; ():1.

Chicago/Turabian Style

Chenglu Peng; Zhifeng Sun; Lei Wang; Yingshuang Shu; Mengchu He; Hongyan Ding; Yu Li; Xichun Wang; Shibin Feng; Jinchun Li; JinJie Wu. 2020. "Glycinin-induced porcine IPEC-J2 cells damage via the NF-κB/MAPK signaling pathway." , no. : 1.

Journal article
Published: 27 March 2020 in Toxicology in Vitro
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Deoxynivalenol (DON), a type B trichothecene mycotoxin mainly affects the health status of pigs and reduced their growth. This study aimed to determine the effects of PI3K/Akt/mTOR pathway on DON-induced autophagy of piglet hippocampal nerve cells (PHNCs), and the relationship between autophagy and apoptosis. The effects of DON on autophagy of PHNCs were examined by cell morphology, cell viability, apoptosis rate, electron microscopy, transient transfection of GFP-LC3 plasmid, immunofluorescence and expression of autophagy-related genes and proteins. The relationship between autophagy and cell apoptosis was analyzed by western blotting, CCK-8 and flow cytometry. The results indicated that, DON inhibited the proliferation of PHNCs and significantly changed cell morphology, and induced apoptosis and autophagy. The expression levels of LC3 protein and gene increased, while the expression levels of PI3K/Akt/mTOR pathway-related genes and proteins decreased, when the concentration of DON increased. Activation of autophagy significantly increased cell viability, reduced apoptosis rate, inhibits autophagy significantly, reduced cell activity and increased apoptosis rate. This data demonstrated that DON exerts certain toxic effect on PHNCs, induced apoptosis and autophagy. PI3K/Akt/mTOR signaling pathway plays a negative regulatory role in DON-induced autophagy of PHNCs. At the same time, autophagy plays a protective role in DON-induced PHNCs injury.

ACS Style

Xichun Wang; Xiaoyan Chu; Li Cao; Jie Zhao; Lei Zhu; Sajid Ur Rahman; Zhen Hu; Yafei Zhang; Shibin Feng; Yu Li; JinJie Wu. The role and regulatory mechanism of autophagy in hippocampal nerve cells of piglet damaged by deoxynivalenol. Toxicology in Vitro 2020, 66, 104837 .

AMA Style

Xichun Wang, Xiaoyan Chu, Li Cao, Jie Zhao, Lei Zhu, Sajid Ur Rahman, Zhen Hu, Yafei Zhang, Shibin Feng, Yu Li, JinJie Wu. The role and regulatory mechanism of autophagy in hippocampal nerve cells of piglet damaged by deoxynivalenol. Toxicology in Vitro. 2020; 66 ():104837.

Chicago/Turabian Style

Xichun Wang; Xiaoyan Chu; Li Cao; Jie Zhao; Lei Zhu; Sajid Ur Rahman; Zhen Hu; Yafei Zhang; Shibin Feng; Yu Li; JinJie Wu. 2020. "The role and regulatory mechanism of autophagy in hippocampal nerve cells of piglet damaged by deoxynivalenol." Toxicology in Vitro 66, no. : 104837.

Journal article
Published: 27 March 2020 in Animals
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Dairy cows usually experience negative energy balance coupled with an increased incidence of fatty liver during the periparturient period. The purpose of this study was to investigate the effect of hepatic steatosis on the expression of the sirtuin 1 (SIRT1), along with the target mRNA and protein expressions and activities related to lipid metabolism in liver tissue. Control cows (n = 6, parity 3.0 ± 2.0, milk production 28 ± 7 kg/d) and mild fatty liver cows (n = 6, parity 2.3 ± 1.5, milk production 20 ± 6 kg/d) were retrospectively selected based on liver triglycerides (TG) content (% wet liver). Compared with the control group, fatty liver cows had greater concentrations of cholesterol and TG along with the typically vacuolated appearance and greater lipid droplets in the liver. Furthermore, fatty liver cows had greater mRNA and protein abundance related to hepatic lipid synthesis proteins sterol regulatory element binding proteins (SREBP-1c), long-chain acyl-CoA synthetase (ACSL), acyl-CoA carbrolase (ACC) and fatty acid synthase (FAS) and lipid transport proteins Liver fatty acid binding protein (L-FABP), apolipoprotein E (ApoE), low density lipoprotein receptor (LDLR) and microsomal TG transfer protein (MTTP) (p < 0.05). However, they had lower mRNA and protein abundance associated with fatty acid β-oxidation proteins SIRT1, peroxisome proliferator-activated receptor co-activator-1 (PGC-1α), peroxisome proliferator–activated receptor-α (PPARα), retinoid X receptor (RXRα), acyl-CoA 1 (ACO), carnitine palmitoyltransferase 1 (CPT1), carnitine palmitoyltransferase 2 (CPT2) and long- and medium-chain 3-hydroxyacyl-CoA dehydrogenases (LCAD) (p < 0.05). Additionally, mRNA abundance and enzyme activity of enzymes copper/zinc superoxide dismutase (Cu/Zn SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and manganese superoxide dismutase (Mn SOD) decreased and mRNA and protein abundance of p45 nuclear factor-erythroid 2 (p45 NF-E2)-related factor 1 (Nrf1), mitochondrial transcription factor A (TFAM) decreased (p < 0.05). Lower enzyme activities of SIRT1, PGC-1α, Cu/Zn SOD, CAT, GSH-Px, SREBP-1c and Mn SOD (p < 0.05) and concentration of reactive oxygen species (ROS) were observed in dairy cows with fatty liver. These results demonstrate that decreased SIRT1 associated with hepatic steatosis promotes hepatic fatty acid synthesis and inhibits fatty acid β-oxidation. Hence, SIRT1 may represent a novel therapeutic target for the treatment of the fatty liver disease in dairy cows.

ACS Style

Yu Li; Suping Zou; Hongyan Ding; Ning Hao; Yingying Huang; Jishun Tang; Jianbo Cheng; Shibin Feng; Jinchun Li; Xichun Wang; JinJie Wu. Low Expression of Sirtuin 1 in the Dairy Cows with Mild Fatty Liver Alters Hepatic Lipid Metabolism. Animals 2020, 10, 560 .

AMA Style

Yu Li, Suping Zou, Hongyan Ding, Ning Hao, Yingying Huang, Jishun Tang, Jianbo Cheng, Shibin Feng, Jinchun Li, Xichun Wang, JinJie Wu. Low Expression of Sirtuin 1 in the Dairy Cows with Mild Fatty Liver Alters Hepatic Lipid Metabolism. Animals. 2020; 10 (4):560.

Chicago/Turabian Style

Yu Li; Suping Zou; Hongyan Ding; Ning Hao; Yingying Huang; Jishun Tang; Jianbo Cheng; Shibin Feng; Jinchun Li; Xichun Wang; JinJie Wu. 2020. "Low Expression of Sirtuin 1 in the Dairy Cows with Mild Fatty Liver Alters Hepatic Lipid Metabolism." Animals 10, no. 4: 560.

Preprint content
Published: 12 March 2020
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Background: Glycinin, a protein found in soybean, is a human and animal allergen. It been previously shown to damage the intestinal barrier. However, its mechanisms of action remain unclear. Therefore, in this study, the intestinal porcine epithelial cell line IPEC-J2 was used to study the effect of glycinin concentration on the intestinal epithelium and identify the related signaling pathways. Results: IPEC-J2 cells were divided into seven treatment groups and a control group; the cells were treated for 24 h with 1, 5, or 10 mg/mL glycinin or with 5 mg/mL glycinin after 30 min of pre-treatment with 1 μmol/L nuclear factor-kappa B (NF-κB) inhibitor (pyrrolidine dithiocarbamate), inducible nitric oxide synthase inhibitor (N-ω-nitro-l-arginine methyl ester), Jun N-terminal kinase (JNK) inhibitor (SP600125), or p38 inhibitor (SB202190). A series of molecular and biochemical experiments revealed that the levels of NF-κB, p38, and JNK, as well as their downstream proteins, increased after the treatment compared with those in the control group.

ACS Style

Chenglu Peng; Zhifeng Sun; Lei Wang; Yingshuang Shu; Mengchu He; Hongyan Ding; Yu Li; Xichun Wang; Shibin Feng; Jinchun Li; JinJie Wu. Glycinin-induced porcine IPEC-J2 cell damage via the NF-κB/MAPK signaling pathway. 2020, 1 .

AMA Style

Chenglu Peng, Zhifeng Sun, Lei Wang, Yingshuang Shu, Mengchu He, Hongyan Ding, Yu Li, Xichun Wang, Shibin Feng, Jinchun Li, JinJie Wu. Glycinin-induced porcine IPEC-J2 cell damage via the NF-κB/MAPK signaling pathway. . 2020; ():1.

Chicago/Turabian Style

Chenglu Peng; Zhifeng Sun; Lei Wang; Yingshuang Shu; Mengchu He; Hongyan Ding; Yu Li; Xichun Wang; Shibin Feng; Jinchun Li; JinJie Wu. 2020. "Glycinin-induced porcine IPEC-J2 cell damage via the NF-κB/MAPK signaling pathway." , no. : 1.

Journal article
Published: 05 March 2020 in Ecotoxicology and Environmental Safety
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Deoxynivalenol(DON) has broad toxicity in livestock, but we know little about its neurotoxic mechanisms. We investigated DON neurotoxicity in the cerebral cortex, cerebellum, and hippocampus of “Duroc × Landrace × Yokshire” piglets. Control piglets were fed a basal diet, while those in low- and high-treatment groups were fed diets with 1.3 mg/kg and 2.2 mg/kg DON, respectively. After a 60 d trial, scanning electron microscopy revealed the destruction of hippocampal cell ultrastructure. As DON concentrations increased, oxidative damage also increased in the cerebral cortex, cerebellum, and hippocampus. Norepinephrine and 5-hydroxytryptamine concentrations tended to increase, whereas dopamine and γ-aminobutyric acid concentrations decreased. We also observed an increase in calcium concentration, relative mRNA expression of calcium/calmodulin-dependent protein kinase II (CaMKII), and CaMKII phosphorylation. However, calmodulin (CaM) mRNA and protein content decreased. Overall, our results suggest that DON acts through the Ca2+/CaM/CaMKII signaling pathway to influence cerebral lipid peroxidation and neurotransmitter levels.

ACS Style

Xichun Wang; Xiaofang Chen; Li Cao; Lei Zhu; Yafei Zhang; Xiaoyan Chu; Dianfeng Zhu; Sajid Ur Rahman; Chenglu Peng; Shibin Feng; Yu Li; JinJie Wu. Mechanism of deoxynivalenol-induced neurotoxicity in weaned piglets is linked to lipid peroxidation, dampened neurotransmitter levels, and interference with calcium signaling. Ecotoxicology and Environmental Safety 2020, 194, 110382 .

AMA Style

Xichun Wang, Xiaofang Chen, Li Cao, Lei Zhu, Yafei Zhang, Xiaoyan Chu, Dianfeng Zhu, Sajid Ur Rahman, Chenglu Peng, Shibin Feng, Yu Li, JinJie Wu. Mechanism of deoxynivalenol-induced neurotoxicity in weaned piglets is linked to lipid peroxidation, dampened neurotransmitter levels, and interference with calcium signaling. Ecotoxicology and Environmental Safety. 2020; 194 ():110382.

Chicago/Turabian Style

Xichun Wang; Xiaofang Chen; Li Cao; Lei Zhu; Yafei Zhang; Xiaoyan Chu; Dianfeng Zhu; Sajid Ur Rahman; Chenglu Peng; Shibin Feng; Yu Li; JinJie Wu. 2020. "Mechanism of deoxynivalenol-induced neurotoxicity in weaned piglets is linked to lipid peroxidation, dampened neurotransmitter levels, and interference with calcium signaling." Ecotoxicology and Environmental Safety 194, no. : 110382.

Original research article
Published: 12 January 2020 in Journal of Cellular Physiology
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Deoxynivalenol (DON) is a major mycotoxin from the trichothecene family of mycotoxins produced by Fusarium fungi. It can cause a variety of adverse effects on human and farm animal health. Here, we determined the effect of DON on the Class III phosphatidylinositol 3‐kinase (PIK3C3)/beclin 1/B cell lymphoma‐2 (Bcl‐2) pathway in PC12 cells and the relationship between autophagy and apoptosis. The effects of DON were evaluated based on the apoptosis ratio; the typical indicators of autophagy, including cellular morphology, acridine orange‐ and monodansylcadaverine‐labeled vacuoles, green fluorescent protein–microtubule associated protein 1 light chain 3 (LC3) localization, and LC3 immunofluorescence; and the expression of key autophagy‐related genes and proteins, that is, PIK3C3, beclin 1, Bcl‐2, LC3, and p62. The relationship between autophagy and apoptosis was analyzed by western blot analysis and flow cytometry. DON‐induced PC12 cell morphological changes and autophagy significantly. PIK3C3, beclin 1, and LC3 increased in tandem with the DON concentration used; Bcl‐2 and p62 expression decreased as DON concentrations increased. Moreover, the PIK3C3/beclin 1/Bcl‐2 signaling pathway played a role in DON‐induced autophagy. Our findings suggest that DON can induce autophagy by activating the PIK3C3/beclin 1/Bcl‐2 signaling pathway and that autophagy may play a positive role in reducing DON‐induced apoptosis.

ACS Style

Xichun Wang; Yunjing Jiang; Lei Zhu; Li Cao; Wei Xu; Sajid Ur Rahman; Shibin Feng; Yu Li; JinJie Wu. Autophagy protects PC12 cells against deoxynivalenol toxicity via the Class III PI3K/beclin 1/Bcl‐2 pathway. Journal of Cellular Physiology 2020, 235, 1 .

AMA Style

Xichun Wang, Yunjing Jiang, Lei Zhu, Li Cao, Wei Xu, Sajid Ur Rahman, Shibin Feng, Yu Li, JinJie Wu. Autophagy protects PC12 cells against deoxynivalenol toxicity via the Class III PI3K/beclin 1/Bcl‐2 pathway. Journal of Cellular Physiology. 2020; 235 (11):1.

Chicago/Turabian Style

Xichun Wang; Yunjing Jiang; Lei Zhu; Li Cao; Wei Xu; Sajid Ur Rahman; Shibin Feng; Yu Li; JinJie Wu. 2020. "Autophagy protects PC12 cells against deoxynivalenol toxicity via the Class III PI3K/beclin 1/Bcl‐2 pathway." Journal of Cellular Physiology 235, no. 11: 1.

Articles
Published: 29 December 2019 in Food and Agricultural Immunology
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β-Conglycinin and glycinin are known to induce various allergic reactions, however, but little is known about the mechanism underlying the development of allergy to soybean antigen proteins. In this study, porcine intestinal epithelial cells (IPEC-J2) were used to investigate the effects of soybean antigen proteins, β-conglycinin and glycinin, on cells to determine whether the caspase-3/mitochondrion-regulated apoptotic pathway underlies the allergic reaction. IPEC-J2 cells were treated with different concentrations (0, 5, and 10 mg mL−1) of β-conglycinin or glycinin, and 50 μM z-DEVD-FMK (a caspase-3 inhibitor). The results show that the apoptosis rate, mitochondrion-regulated mRNA and protein expression levels, caspase-3 activation, cyt-c release, cytoskeleton and tight junction protein expression, mitochondrial membrane potential depolarization and mitochondrial injury were significantly aggravated with cultured in increasing concentrations of β-conglycinin or glycinin. While these effects were inhibited by application of the caspase-3 inhibitor. Thus, we concluded that β-conglycinin and glycinin cause IPEC-J2 cell apoptosis via the caspase-3/mitochondrion-regulated apoptotic pathway.

ACS Style

Chenglu Peng; Zhifeng Sun; Lei Wang; Yingshuang Shu; Mengchu He; Hongyan Ding; Yu Li; Xichun Wang; Shibin Feng; Jinchun Li; JinJie Wu. Soybean antigen protein induces caspase-3/mitochondrion-regulated apoptosis in IPEC-J2 cells. Food and Agricultural Immunology 2019, 31, 100 -119.

AMA Style

Chenglu Peng, Zhifeng Sun, Lei Wang, Yingshuang Shu, Mengchu He, Hongyan Ding, Yu Li, Xichun Wang, Shibin Feng, Jinchun Li, JinJie Wu. Soybean antigen protein induces caspase-3/mitochondrion-regulated apoptosis in IPEC-J2 cells. Food and Agricultural Immunology. 2019; 31 (1):100-119.

Chicago/Turabian Style

Chenglu Peng; Zhifeng Sun; Lei Wang; Yingshuang Shu; Mengchu He; Hongyan Ding; Yu Li; Xichun Wang; Shibin Feng; Jinchun Li; JinJie Wu. 2019. "Soybean antigen protein induces caspase-3/mitochondrion-regulated apoptosis in IPEC-J2 cells." Food and Agricultural Immunology 31, no. 1: 100-119.

Journal article
Published: 20 December 2019 in The Journal of Nutritional Biochemistry
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Green tea polyphenols (GTPs) exhibit beneficial effects towards obesity and intestinal inflammation; however, the mechanisms and association with gut microbiota are unclear. We examined the role of the gut microbiota of GTPs treatment for obesity and inflammation. Canines were fed either a normal diet or high-fat diet with low (0.48% g/kg), medium (0.96% g/kg), or high (1.92% g/kg), doses of GTPs for 18 weeks. GTPs decreased the relative abundance of Bacteroidetes and Fusobacteria and increased the relative abundance of Firmicutes as revealed by 16S rRNA gene sequencing analysis. The relative proportion of Acidaminococcus, Anaerobiospirillum, Anaerovibrio, Bacteroides, Blautia, Catenibactetium, Citrobacter, Clostridium, Collinsella, and Escherichia were significantly associated with GTPs-induced weight loss. GTPs significantly (p<0.01) decreased expression levels of inflammatory cytokines, including TNF-α, IL-6, and IL-1β, and inhibited induction of the TLR4 signaling pathway compared with high-fat diet. We show that the therapeutic effects of GTPs correspond with changes in gut microbiota and intestinal inflammation, which may be related to the anti-inflammatory and anti-obesity mechanisms of GTPs.

ACS Style

Yu Li; Sajid Ur Rahman; Yingying Huang; Yafei Zhang; Pengfei Ming; Lei Zhu; Xiaoyan Chu; Jinchun Li; Shibin Feng; Xichun Wang; JinJie Wu. Green tea polyphenols decrease weight gain, ameliorate alteration of gut microbiota, and mitigate intestinal inflammation in canines with high-fat-diet-induced obesity. The Journal of Nutritional Biochemistry 2019, 78, 108324 .

AMA Style

Yu Li, Sajid Ur Rahman, Yingying Huang, Yafei Zhang, Pengfei Ming, Lei Zhu, Xiaoyan Chu, Jinchun Li, Shibin Feng, Xichun Wang, JinJie Wu. Green tea polyphenols decrease weight gain, ameliorate alteration of gut microbiota, and mitigate intestinal inflammation in canines with high-fat-diet-induced obesity. The Journal of Nutritional Biochemistry. 2019; 78 ():108324.

Chicago/Turabian Style

Yu Li; Sajid Ur Rahman; Yingying Huang; Yafei Zhang; Pengfei Ming; Lei Zhu; Xiaoyan Chu; Jinchun Li; Shibin Feng; Xichun Wang; JinJie Wu. 2019. "Green tea polyphenols decrease weight gain, ameliorate alteration of gut microbiota, and mitigate intestinal inflammation in canines with high-fat-diet-induced obesity." The Journal of Nutritional Biochemistry 78, no. : 108324.

Journal article
Published: 16 December 2019 in Toxins
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The aim of this study was to investigate the effects of deoxynivalenol (DON) exposure on the inflammatory injury nuclear factor kappa-B (NF-κB) pathway in intestinal epithelial cells (IPEC-J2 cells) of pig. The different concentrations of DON (0, 125, 250, 500, 1000, 2000 ng/mL) were added to the culture solution for treatment. The NF-κB pathway inhibitor pyrrolidine dithiocarbamate (PDTC) was used as a reference. The results showed that when the DON concentration increased, the cell density decreased and seemed damaged. With the increase of DON concentration in the culture medium, the action of diamine oxidase (DAO) in the culture supernatant also increased. The activities of IL-6, TNF-α, and NO in the cells were increased with the increasing DON concentration. The relative mRNA expression of IL-1β and IL-6 were increased in the cells. The mRNA relative expression of NF-κB p65, IKKα, and IKKβ were upregulated with the increasing of DON concentration, while the relative expression of IκB-α mRNA was downregulated. At the same time, the expression of NF-κB p65 protein increased gradually in the cytoplasm and nucleus with a higher concentration of DON. These results showed that DON could change the morphology of IPEC-J2 cells, destroy its submicroscopic structure, and enhance the permeability of cell membrane, as well as upregulate the transcription of some inflammatory factors and change the expression of NF-κB-related gene or protein in cells.

ACS Style

Xichun Wang; Yafei Zhang; Jie Zhao; Li Cao; Lei Zhu; Yingying Huang; Xiaofang Chen; Sajid Ur Rahman; Shibin Feng; Yu Li; JinJie Wu. Deoxynivalenol Induces Inflammatory Injury in IPEC-J2 Cells via NF-κB Signaling Pathway. Toxins 2019, 11, 733 .

AMA Style

Xichun Wang, Yafei Zhang, Jie Zhao, Li Cao, Lei Zhu, Yingying Huang, Xiaofang Chen, Sajid Ur Rahman, Shibin Feng, Yu Li, JinJie Wu. Deoxynivalenol Induces Inflammatory Injury in IPEC-J2 Cells via NF-κB Signaling Pathway. Toxins. 2019; 11 (12):733.

Chicago/Turabian Style

Xichun Wang; Yafei Zhang; Jie Zhao; Li Cao; Lei Zhu; Yingying Huang; Xiaofang Chen; Sajid Ur Rahman; Shibin Feng; Yu Li; JinJie Wu. 2019. "Deoxynivalenol Induces Inflammatory Injury in IPEC-J2 Cells via NF-κB Signaling Pathway." Toxins 11, no. 12: 733.

Journal article
Published: 14 November 2019 in Toxins
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Deoxynivalenol (DON) is highly toxic to animals and humans, but pigs are most sensitive to it. The porcine mucosal injury related mechanism of DON is not yet fully clarified. Here, we investigated DON-induced injury in the intestinal tissues of piglet. Thirty weanling piglets [(Duroc × Landrace) × Yorkshire] were randomly divided into three groups according to single factor experimental design (10 piglets each group). Piglets were fed a basal diet in the control group, while low and high dose groups were fed a DON diet (1300 and 2200 μg/kg, respectively) for 60 days. Scanning electron microscopy results indicated that the ultrastructure of intestinal epithelial cells in the DON-treated group was damaged. The distribution and optical density (OD) values of zonula occludens 1 (ZO-1) protein in the intestinal tissues of DON-treated groups were decreased. At higher DON dosage, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α mRNA levels were elevated in the intestinal tissues. The mRNA and protein levels of NF-κB p65, IκB-α, IKKα/β, iNOS, and COX-2 in the small intestinal mucosa were abnormally altered with an increase in DON concentration. These results indicate that DON can persuade intestinal damage and inflammatory responses in piglets via the nuclear factor-κB signaling pathway.

ACS Style

Xi-Chun Wang; Ya-Fei Zhang; Li Cao; Lei Zhu; Ying-Ying Huang; Xiao-Fang Chen; Xiao-Yan Chu; Dian-Feng Zhu; Sajid Ur Rahman; Shi-Bin Feng; Yu Li; Jin-Jie Wu. Deoxynivalenol Induces Intestinal Damage and Inflammatory Response through the Nuclear Factor-κB Signaling Pathway in Piglets. Toxins 2019, 11, 663 .

AMA Style

Xi-Chun Wang, Ya-Fei Zhang, Li Cao, Lei Zhu, Ying-Ying Huang, Xiao-Fang Chen, Xiao-Yan Chu, Dian-Feng Zhu, Sajid Ur Rahman, Shi-Bin Feng, Yu Li, Jin-Jie Wu. Deoxynivalenol Induces Intestinal Damage and Inflammatory Response through the Nuclear Factor-κB Signaling Pathway in Piglets. Toxins. 2019; 11 (11):663.

Chicago/Turabian Style

Xi-Chun Wang; Ya-Fei Zhang; Li Cao; Lei Zhu; Ying-Ying Huang; Xiao-Fang Chen; Xiao-Yan Chu; Dian-Feng Zhu; Sajid Ur Rahman; Shi-Bin Feng; Yu Li; Jin-Jie Wu. 2019. "Deoxynivalenol Induces Intestinal Damage and Inflammatory Response through the Nuclear Factor-κB Signaling Pathway in Piglets." Toxins 11, no. 11: 663.

Article
Published: 07 November 2019 in Chemical Research in Chinese Universities
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The anti-inflammatory activity of tea polyphenols(TPs) in RAW264.7 macrophages stimulated by lipopolysaccharide(LPS) was investigated in this paper. RAW264.7 macrophages were treated with different concentrations of TP(0, 12.5, 25, 50, 100, and 200 µg/mL) and then stimulated by LPS. Another blank control group was set up. The expression of pro-inflammatory cytokines associated with the nuclear factor-kappa B(NF-κB) signaling pathway was investigated before and after TP treatment. Pretreatment of RAW264.7 cells with TP decreased the expression of tumor necrosis factor-α(TNF-α), interleukin-6(IL-6) and interleukin 1 beta(IL-1β) pro-inflammatory cytokines. In addition, TP inhibited the phosphorylation of p65 and IκB by blocking the phosphorylation and the degradation of NF-κB inhibitor protein. In conclusion, TP exerts anti-inflammatory effects by regulating the release of inflammatory mediators via the NF-κB signaling pathway.

ACS Style

Siyi Su; Xiaoyu Li; Xu Guo; Ruiming Zhou; Manman Li; Pengfei Ming; Yingying Huang; Sajid Ur Rahman; Hongyan Ding; Shibin Feng; Jinchun Li; Xichun Wang; Yu Li; JinJie Wu. Tea Polyphenols Reducing Lipopolysaccharide-induced Inflammatory Responses in RAW264.7 Macrophages via NF-κB Pathway. Chemical Research in Chinese Universities 2019, 35, 1105 -1110.

AMA Style

Siyi Su, Xiaoyu Li, Xu Guo, Ruiming Zhou, Manman Li, Pengfei Ming, Yingying Huang, Sajid Ur Rahman, Hongyan Ding, Shibin Feng, Jinchun Li, Xichun Wang, Yu Li, JinJie Wu. Tea Polyphenols Reducing Lipopolysaccharide-induced Inflammatory Responses in RAW264.7 Macrophages via NF-κB Pathway. Chemical Research in Chinese Universities. 2019; 35 (6):1105-1110.

Chicago/Turabian Style

Siyi Su; Xiaoyu Li; Xu Guo; Ruiming Zhou; Manman Li; Pengfei Ming; Yingying Huang; Sajid Ur Rahman; Hongyan Ding; Shibin Feng; Jinchun Li; Xichun Wang; Yu Li; JinJie Wu. 2019. "Tea Polyphenols Reducing Lipopolysaccharide-induced Inflammatory Responses in RAW264.7 Macrophages via NF-κB Pathway." Chemical Research in Chinese Universities 35, no. 6: 1105-1110.

Preprint
Published: 23 October 2019
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Background: Deoxynivalenol (DON) is a common trichothecene mycotoxin found throughout the world. DON has broad toxicity in animals and humans. Its neurotoxicity in vitro, however, is still unclear. This study was designed to investigate the hypothesis that DON toxicity in neurons occurs via the mitochondrial apoptotic pathway. Results: Using piglet hippocampal nerve cells (PHNCs), we evaluated the effects of varying concentrations of DON on typical indicators of apoptosis. The results obtained demonstrated that DON treatment inhibited PHNC proliferation and led to morphological, biochemical, and transcriptional changes consistent with apoptosis, including decreased mitochondrial membrane potential, mitochondrial release of CYCS and AIF, and increased abundance of active cleaved-caspase-9 and cleaved-caspase-3. Increasing concentrations of DON led to decreased Bcl-2 expression and increased expression of Bax and Bid, which in turn increased transcriptional activity of the transcription factors AIF and P53. Addition of a caspase-8 inhibitor abrogated these effects. Conclusion: These data reveal that DON induces apoptosis in PHNCs via the mitochondrial apoptosis pathway, and that caspase-8 plays an important role during apoptosis regulation.

ACS Style

JinJie Wu; Xichun Wang; Yunjing Jiang; Lei Zhu; Li Cao; Wei Xu; Xiaoyan Chu; Yafei Zhang; Sajid Ur Rahman; Shibin Feng; Yu Li. Deoxynivalenol induces caspase-8-mediated apoptosis through the mitochondrial pathway in hippocampal nerve cells of piglet. 2019, 1 .

AMA Style

JinJie Wu, Xichun Wang, Yunjing Jiang, Lei Zhu, Li Cao, Wei Xu, Xiaoyan Chu, Yafei Zhang, Sajid Ur Rahman, Shibin Feng, Yu Li. Deoxynivalenol induces caspase-8-mediated apoptosis through the mitochondrial pathway in hippocampal nerve cells of piglet. . 2019; ():1.

Chicago/Turabian Style

JinJie Wu; Xichun Wang; Yunjing Jiang; Lei Zhu; Li Cao; Wei Xu; Xiaoyan Chu; Yafei Zhang; Sajid Ur Rahman; Shibin Feng; Yu Li. 2019. "Deoxynivalenol induces caspase-8-mediated apoptosis through the mitochondrial pathway in hippocampal nerve cells of piglet." , no. : 1.

Journal article
Published: 18 July 2019 in Journal of Agricultural and Food Chemistry
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Soybean allergy is a serious health risk to humans and animals; β-conglycinin is the primary antigenic protein in soybean. Intestinal porcine epithelial (IPEC-J2) cells were used as an in vitro physiological model of the intestinal epithelium to study the effects of different concentrations of soybean antigen protein β-conglycinin to identify the involved signaling pathways. The cells were divided into eight groups and either untreated or treated with different concentrations of β-conglycinin, pyrrolidine dithiocarbamate (PDTC), Nω-nitro-l-arginine methyl ester hydrochloride (l-NAME), SP600125, and SB202190 either alone or in combination. The cells were incubated with 1, 5, and 10 mg·mL-1 β-conglycinin or 5 mg·mL-1 β-conglycinin and 1 μmol·L-1 nuclear factor κB (NF-κB) inhibitor (PDTC), inducible nitric oxide synthase inhibitor (l-NAME), c-Jun N-terminal kinase (JNK) inhibitor (SP600125), and p38 inhibitor (SB202190) for 24 h, separately; controls were left untreated. The mRNA, protein, and phosphorylation levels of NF-κB, p38, and JNK were higher in the treated groups than in the control group. β-Conglycinin decreased tight junction distribution, destroyed the cytoskeleton of IPEC-J2 cells, and caused cell death. After the addition of the inhibitors, β-conglycinin-induced IPEC-J2 cell damage was significantly reduced. β-Conglycinin caused damage to IPEC-J2 cells via the mitogen-activated protein kinase/NF-κB signaling pathway. The results of this study are crucial for exploring the mechanisms underlying allergic reactions caused by soybean antigen proteins.

ACS Style

Chenglu Peng; Xuedong Ding; Lei Zhu; Mengchu He; Yingshuang Shu; Yu Zhang; Yu Li; Xichun Wang; Shibin Feng; Jinchun Li; JinJie Wu. β-Conglycinin-Induced Intestinal Porcine Epithelial Cell Damage via the Nuclear Factor κB/Mitogen-Activated Protein Kinase Signaling Pathway. Journal of Agricultural and Food Chemistry 2019, 67, 9009 -9021.

AMA Style

Chenglu Peng, Xuedong Ding, Lei Zhu, Mengchu He, Yingshuang Shu, Yu Zhang, Yu Li, Xichun Wang, Shibin Feng, Jinchun Li, JinJie Wu. β-Conglycinin-Induced Intestinal Porcine Epithelial Cell Damage via the Nuclear Factor κB/Mitogen-Activated Protein Kinase Signaling Pathway. Journal of Agricultural and Food Chemistry. 2019; 67 (32):9009-9021.

Chicago/Turabian Style

Chenglu Peng; Xuedong Ding; Lei Zhu; Mengchu He; Yingshuang Shu; Yu Zhang; Yu Li; Xichun Wang; Shibin Feng; Jinchun Li; JinJie Wu. 2019. "β-Conglycinin-Induced Intestinal Porcine Epithelial Cell Damage via the Nuclear Factor κB/Mitogen-Activated Protein Kinase Signaling Pathway." Journal of Agricultural and Food Chemistry 67, no. 32: 9009-9021.

Journal article
Published: 30 May 2019 in BMC Veterinary Research
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Breast cancer resistance protein (BCRP) and multidrug resistance protein 4 (MRP4) are involved in uric acid excretion in humans and mice. Despite evidence suggesting that renal proximal tubular epithelial cells participate in uric acid excretion in chickens, the roles of BCRP and MRP4 therein remain unclear. This study evaluated the relationship between BCRP and MRP4 expression and renal function in chickens. Sixty laying hens were randomly divided into four treatment groups: a control group (NC) fed a basal diet; a sulfonamide-treated group (SD) fed the basal diet and supplemented with sulfamonomethoxine sodium via drinking water (8 mg/L); a fish meal group (FM) fed the basal diet supplemented with 16% fishmeal; and a uric acid injection group (IU) fed the basal diet and intraperitoneally injected with uric acid (250 mg/kg body weight). The results showed that serum uric acid, creatinine, and blood urea nitrogen levels were significantly higher in the SD and IU, but not FM, than in the NC groups. Renal tubular epithelial cells in the SD and IU groups were damaged. Liver BCRP and MRP4 mRNA and protein levels were significantly decreased in the SD and IU groups, but slightly increased in the FM group. In the SD group, BCRP and MRP4 were significantly increased in the ileum and slightly increased in the kidney. In the FM group, BCRP and MRP4 were significantly increased in the kidney and slightly increased in the ileum. In the IU group, BCRP and MRP4 were significantly increased in the kidney and ileum. BCRP and MRP4 expression in the jejunum was not affected by the treatments. Together, these results demonstrate that BCRP and MRP4 are involved in renal and intestinal uric acid excretion in chickens and that BCRP is positively related to MRP4 expression. Further, impairment of renal function results in an increase in serum uric acid as well as a compensatory increase in BCRP and MRP4 in the ileum; however, under normal renal function, renal BCRP and MRP4 are the main regulators of uric acid excretion.

ACS Style

Xuedong Ding; Manman Li; Chenglu Peng; Zhi Wang; Shoufa Qian; Yuying Ma; Tianyi Fang; Shibin Feng; Yu Li; Xichun Wang; Jinchun Li; JinJie Wu. Uric acid transporters BCRP and MRP4 involved in chickens uric acid excretion. BMC Veterinary Research 2019, 15, 180 .

AMA Style

Xuedong Ding, Manman Li, Chenglu Peng, Zhi Wang, Shoufa Qian, Yuying Ma, Tianyi Fang, Shibin Feng, Yu Li, Xichun Wang, Jinchun Li, JinJie Wu. Uric acid transporters BCRP and MRP4 involved in chickens uric acid excretion. BMC Veterinary Research. 2019; 15 (1):180.

Chicago/Turabian Style

Xuedong Ding; Manman Li; Chenglu Peng; Zhi Wang; Shoufa Qian; Yuying Ma; Tianyi Fang; Shibin Feng; Yu Li; Xichun Wang; Jinchun Li; JinJie Wu. 2019. "Uric acid transporters BCRP and MRP4 involved in chickens uric acid excretion." BMC Veterinary Research 15, no. 1: 180.

Original article
Published: 15 January 2019 in Animal Science Journal
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Soybeans are used increasingly in food products because of their health benefits. In this study, we investigated the effect of soybean antigen protein on weaned piglet intestine. Seventy piglets were randomly divided into seven groups with 10 piglets each. At 7 and 14 days of age, groups A–C were injected with saline, and D–G were intramuscularly injected with or orally administered 7S or 11S. Groups B–G were artificially sensitized by dietary 7S or 11S. At 27 days, the small intestinal tissues were collected to determine levels of histamine, sIgA protein, and IgA mRNA. Histamine in B–G was significantly decreased in the duodenum and ileum. Moreover, sIgA expression was higher in all groups than in A, with B/C>D–G and F/G>D/E; the trend in IgA expression was similar. Collectively, these results indicated that soybean antigen protein‐immunizing agents decrease sIgA and IgA levels. Additionally, the effect of injection immunization occurred prior to that of oral immunization.

ACS Style

Chenglu Peng; Xuebing Tang; Yingshuang Shu; Mengchu He; Xiaodong Xia; Yu Zhang; Chengming Cao; Yu Li; Shibin Feng; Xichun Wang; JinJie Wu. Effects of 7S and 11S on the intestine of weaned piglets after injection and oral administration of soybean antigen protein. Animal Science Journal 2019, 90, 393 -400.

AMA Style

Chenglu Peng, Xuebing Tang, Yingshuang Shu, Mengchu He, Xiaodong Xia, Yu Zhang, Chengming Cao, Yu Li, Shibin Feng, Xichun Wang, JinJie Wu. Effects of 7S and 11S on the intestine of weaned piglets after injection and oral administration of soybean antigen protein. Animal Science Journal. 2019; 90 (3):393-400.

Chicago/Turabian Style

Chenglu Peng; Xuebing Tang; Yingshuang Shu; Mengchu He; Xiaodong Xia; Yu Zhang; Chengming Cao; Yu Li; Shibin Feng; Xichun Wang; JinJie Wu. 2019. "Effects of 7S and 11S on the intestine of weaned piglets after injection and oral administration of soybean antigen protein." Animal Science Journal 90, no. 3: 393-400.

Original research article
Published: 27 November 2018 in Journal of Cellular Physiology
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The ketotic cows displayed hepatic lipid metabolic disorder and high blood concentration of glucagon. Importantly, adenosine monophosphate‐activated protein kinase (AMPK) signaling pathway plays an important role in the hepatic lipid homeostasis. Therefore, the aim of this study was to investigate the effect of glucagon on AMPK pathway and its underlying mechanism on lipid metabolism in cow hepatocytes. Cow hepatocytes were cultured and treated with glucagon and AMPK inhibitor (BML‐275). The results showed that glucagon significantly promoted the expression of glucagon receptor and increased the phosphorylation level and activity of AMPKα. Activated AMPKα increased the expression level and transcriptional activity of peroxisome proliferator‐activated receptor α, which further increased the expression of fatty acid oxidation genes and lipid oxidation. Furthermore, activated AMPKα inhibited the expression level and transcriptional activity of sterol regulatory element binding protein‐1c and carbohydrate response element binding protein, which decreased the expression of lipogenic genes, thereby decreasing lipid synthesis. In addition, glucagon also increased the expression of very‐low‐density lipoprotein (VLDL) assembly to export intracellular triglycerides (TG). Consequently, the content of intracellular TG was significantly decreased in cow hepatocytes. These results indicate that glucagon activates the AMPK signaling pathway to increase lipid oxidation and VLDL assembly and decrease lipid synthesis in cow hepatocytes, thereby reducing liver fat accumulation.

ACS Style

Yu Li; Hongyan Ding; Jihong Dong; Sajid Ur Rahman; Shibin Feng; Xichun Wang; JinJie Wu; Zhe Wang; Guowen Liu; Xiaobing Li; Xinwei Li. Glucagon attenuates lipid accumulation in cow hepatocytes through AMPK signaling pathway activation. Journal of Cellular Physiology 2018, 234, 6054 -6066.

AMA Style

Yu Li, Hongyan Ding, Jihong Dong, Sajid Ur Rahman, Shibin Feng, Xichun Wang, JinJie Wu, Zhe Wang, Guowen Liu, Xiaobing Li, Xinwei Li. Glucagon attenuates lipid accumulation in cow hepatocytes through AMPK signaling pathway activation. Journal of Cellular Physiology. 2018; 234 (5):6054-6066.

Chicago/Turabian Style

Yu Li; Hongyan Ding; Jihong Dong; Sajid Ur Rahman; Shibin Feng; Xichun Wang; JinJie Wu; Zhe Wang; Guowen Liu; Xiaobing Li; Xinwei Li. 2018. "Glucagon attenuates lipid accumulation in cow hepatocytes through AMPK signaling pathway activation." Journal of Cellular Physiology 234, no. 5: 6054-6066.