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Yu Li
Department of Veterinary Medicine, College of Animal Science and Technology, Anhui Agricultural University, Hefei 230036, China

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Journal article
Published: 16 July 2021 in Animals
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The objective was to perform a proof-of-principle study to evaluate the effects of methionine (Met) and arginine (Arg) supply on protein abundance of amino acid, insulin signaling, and glutathione metabolism-related proteins in subcutaneous adipose tissue (SAT) explants under ceramide (Ce) challenge. SAT from four lactating Holstein cows was incubated with one of the following media: ideal profile of amino acid as the control (IPAA; Lys:Met 2.9:1, Lys:Arg 2:1), increased Met (incMet; Lys:Met 2.5:1), increased Arg (incArg; Lys:Arg 1:1), or incMet plus incArg (Lys:Met 2.5:1 Lys:Arg 1:1) with or without 100 μM exogenous cell-permeable Ce (N-Acetyl-d-sphingosine). Ceramide stimulation downregulated the overall abundance of phosphorylated (p) protein kinase B (AKT), p-mechanistic target of rapamycin (mTOR), and p-eukaryotic elongation factor 2 (eEF2). Without Ce stimulation, increased Met, Arg, or Met + Arg resulted in lower p-mTOR. Compared with control SAT stimulated with Ce, increased Met, Arg, or Met + Arg resulted in greater activation of mTOR (p-mTOR/total mTOR) and AKT (p-AKT/total AKT), with a more pronounced response due to Arg. The greatest protein abundance of glutathione S-transferase Mu 1 (GSTM1) was detected in response to increased Met supply during Ce stimulation. Ceramide stimulation decreased the overall protein abundance of the Na-coupled neutral amino acid transporter SLC38A1 and branched-chain alpha-ketoacid dehydrogenase kinase (BCKDK). However, compared with controls, increased Met or Arg supply attenuated the downregulation of BCKDK induced by Ce. Circulating ceramides might affect amino acid, insulin signaling, and glutathione metabolism in dairy cow adipose tissue. Further in vivo studies are needed to confirm the role of rumen-protected amino acids in regulating bovine adipose function.

ACS Style

Yusheng Liang; Nana Ma; Danielle Coleman; Fang Liu; Yu Li; Hongyan Ding; Fabiana Cardoso; Claudia Parys; Felipe Cardoso; Juan Loor. Methionine and Arginine Supply Alters Abundance of Amino Acid, Insulin Signaling, and Glutathione Metabolism-Related Proteins in Bovine Subcutaneous Adipose Explants Challenged with N-Acetyl-d-sphingosine. Animals 2021, 11, 2114 .

AMA Style

Yusheng Liang, Nana Ma, Danielle Coleman, Fang Liu, Yu Li, Hongyan Ding, Fabiana Cardoso, Claudia Parys, Felipe Cardoso, Juan Loor. Methionine and Arginine Supply Alters Abundance of Amino Acid, Insulin Signaling, and Glutathione Metabolism-Related Proteins in Bovine Subcutaneous Adipose Explants Challenged with N-Acetyl-d-sphingosine. Animals. 2021; 11 (7):2114.

Chicago/Turabian Style

Yusheng Liang; Nana Ma; Danielle Coleman; Fang Liu; Yu Li; Hongyan Ding; Fabiana Cardoso; Claudia Parys; Felipe Cardoso; Juan Loor. 2021. "Methionine and Arginine Supply Alters Abundance of Amino Acid, Insulin Signaling, and Glutathione Metabolism-Related Proteins in Bovine Subcutaneous Adipose Explants Challenged with N-Acetyl-d-sphingosine." Animals 11, no. 7: 2114.

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: 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.

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.

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: 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.

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.

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.

Journal article
Published: 02 October 2018 in Toxicon
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Deoxynivalenol (DON) is a mycotoxin capable of producing a variety of toxic effects in human and animals. In this study, the effect of DON treatment on cytotoxicity and apoptotic pathways in piglet hippocampal nerve cells (PHNCs) was determined. The effects of DON on cellular morphology, cell activity, lactate dehydrogenase (LDH) release, the protein expression of mitogen-activated protein kinase (MAPK) pathway, and the relative expression of key genes related to apoptosis were evaluated. The results indicated that DON significantly inhibited cellular viability and promoted the release of LDH by damaging the membrane integrity of PHNCs, however, the cellular viability was increased and LDH leakage rate were decreased after adding MAPK inhibitors. DON induced PHNCs apoptosis and phosphorylation of MAPK pathway proteins dose-dependently. The ratios of phospho p-JNK/JNK and p-p38/p38 significantly increased with the increase of DON concentration, while the p-ERK/ERK ratio significantly decreased. In addition, DON upregulated the BAX mRNA level, and downregulated the BCL2 mRNA level. Pre-incubation with inhibitors of JNK (SP600125) and p38 (SB202190) significantly decreases the BAX/BCL2 ratio. However, pre-incubation with the inhibitor of ERK (U0126), significantly increased the BAX/BCL2 ratio. These data demonstrated that DON induces toxic effects and apoptosis in PHNCs via the MAPK signaling pathway.

ACS Style

Xichun Wang; Mengxue Fan; Xiaoyan Chu; Yafei Zhang; Sajid Ur Rahman; Yunjing Jiang; Xiaofang Chen; Dianfeng Zhu; Shibin Feng; Yu Li; JinJie Wu. Deoxynivalenol induces toxicity and apoptosis in piglet hippocampal nerve cells via the MAPK signaling pathway. Toxicon 2018, 155, 1 -8.

AMA Style

Xichun Wang, Mengxue Fan, Xiaoyan Chu, Yafei Zhang, Sajid Ur Rahman, Yunjing Jiang, Xiaofang Chen, Dianfeng Zhu, Shibin Feng, Yu Li, JinJie Wu. Deoxynivalenol induces toxicity and apoptosis in piglet hippocampal nerve cells via the MAPK signaling pathway. Toxicon. 2018; 155 ():1-8.

Chicago/Turabian Style

Xichun Wang; Mengxue Fan; Xiaoyan Chu; Yafei Zhang; Sajid Ur Rahman; Yunjing Jiang; Xiaofang Chen; Dianfeng Zhu; Shibin Feng; Yu Li; JinJie Wu. 2018. "Deoxynivalenol induces toxicity and apoptosis in piglet hippocampal nerve cells via the MAPK signaling pathway." Toxicon 155, no. : 1-8.

Original article
Published: 11 August 2018 in Inflammopharmacology
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Rutin, found widely in traditional Chinese medicine materials, is used to treat eye swelling and pain, hypertension, and hyperlipidemia. In the present study, a mouse mastitis model induced by lipopolysaccharide (LPS) was established to explore rutin’s inhibitory mechanism on mastitis via nuclear factor kappa B (NF-κB) inflammatory signaling and the relationship between NF-κB signaling and endoplasmic reticulum (ER) stress. Mice were divided into six groups: Control group, LPS model group, LPS + rutin (25, 50, and 100 mg/kg) and LPS + dexamethasone (DEX) group. DEX, rutin, and PBS (control and LPS groups) were administered 1 h before and 12 h after perfusion of LPS. After LPS stimulation for 24 h, to evaluate rutin’s therapeutic effect on mastitis, the mammary tissues of each group were collected to detect histopathological injury, tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, and IL-6 mRNA and protein levels; and glucose-regulated protein, 78 kDa (GRP78) protein levels. The protein and mRNA levels of TNF-α, IL-1β, and IL-6 in the LPS + rutin group were significantly lower than those in the LPS model group. Similarly, p50/p105, phosphorylated (p)-p65/p65 and p-inhibitor of nuclear factor kappa b kinase subunit beta (p-IKKβ)/IKKβ ratios in the LPS + rutin group (50 mg/kg) and LPS + rutin group (100 mg/kg) decreased significantly. GRP78 protein expression was significantly higher in LPS + rutin group (100 mg/kg). The structure of mammary tissue became gradually more intact and vacuolization of acini decreased as the rutin concentration increased. The nuclear quantity of p65 in the LPS + rutin group decreased significantly in a rutin dose-dependent manner. Rutin had an anti-inflammatory effect in the LPS-induced mouse mastitis model, manifested by inhibition of NF-κB pathway activation and attenuation of ER stress.

ACS Style

Siyi Su; Xiaoyu Li; Siting Li; Pengfei Ming; Yingying Huang; Yanli Dong; Hongyan Ding; Shibin Feng; Jinchun Li; Xichun Wang; Yu Li; JinJie Wu. Rutin protects against lipopolysaccharide-induced mastitis by inhibiting the activation of the NF-κB signaling pathway and attenuating endoplasmic reticulum stress. Inflammopharmacology 2018, 27, 77 -88.

AMA Style

Siyi Su, Xiaoyu Li, Siting Li, Pengfei Ming, Yingying Huang, Yanli Dong, Hongyan Ding, Shibin Feng, Jinchun Li, Xichun Wang, Yu Li, JinJie Wu. Rutin protects against lipopolysaccharide-induced mastitis by inhibiting the activation of the NF-κB signaling pathway and attenuating endoplasmic reticulum stress. Inflammopharmacology. 2018; 27 (1):77-88.

Chicago/Turabian Style

Siyi Su; Xiaoyu Li; Siting Li; Pengfei Ming; Yingying Huang; Yanli Dong; Hongyan Ding; Shibin Feng; Jinchun Li; Xichun Wang; Yu Li; JinJie Wu. 2018. "Rutin protects against lipopolysaccharide-induced mastitis by inhibiting the activation of the NF-κB signaling pathway and attenuating endoplasmic reticulum stress." Inflammopharmacology 27, no. 1: 77-88.

Review
Published: 27 June 2018 in Nutrients
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Sperm cells are highly sensitive to reactive oxygen species (ROS), which are produced during cellular oxidation. In normal cell biology, ROS levels increase with a decreasing antioxidant response, resulting in oxidative stress which threatens sperm biology. Oxidative stress has numerous effects, including increased apoptosis, reduced motion parameters, and reduced sperm integrity. In this regard, green tea polyphenols (GrTPs) have been reported to possess properties that may increase the quality of male and female gametes, mostly via the capability of catechins to reduce ROS production. GrTPs have antioxidant properties that improve major semen parameters, such as sperm concentration, motility, morphology, DNA damage, fertility rate, and gamete quality. These unique properties of green tea catechins could improve reproductive health and represent an important study area. This exploratory review discusses the therapeutic effects of GrTPs against infertility, their possible mechanisms of action, and recommended supportive therapy for improving fertility in humans and in animals.

ACS Style

Sajid Ur Rahman; Yingying Huang; Lei Zhu; Shibin Feng; Ibrar Muhammad Khan; JinJie Wu; Yu Li; Xichun Wang. Therapeutic Role of Green Tea Polyphenols in Improving Fertility: A Review. Nutrients 2018, 10, 834 .

AMA Style

Sajid Ur Rahman, Yingying Huang, Lei Zhu, Shibin Feng, Ibrar Muhammad Khan, JinJie Wu, Yu Li, Xichun Wang. Therapeutic Role of Green Tea Polyphenols in Improving Fertility: A Review. Nutrients. 2018; 10 (7):834.

Chicago/Turabian Style

Sajid Ur Rahman; Yingying Huang; Lei Zhu; Shibin Feng; Ibrar Muhammad Khan; JinJie Wu; Yu Li; Xichun Wang. 2018. "Therapeutic Role of Green Tea Polyphenols in Improving Fertility: A Review." Nutrients 10, no. 7: 834.

Randomized controlled trial
Published: 17 May 2018 in Toxicon
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During current research, the effects of deoxynivalenol (DON) exposure on cerebral lipid peroxidation, neurotransmitter secretion and calcium homeostasis in chicks were evaluated. One hundred and twenty Hailan chicks (male, 1-day-old) were randomly divided into four groups. Chicks in low, medium and high dose groups were fed with 0.27, 1.68 and 12.21 mg/kg−1 DON respectively by gavage according to feed intake. Chicks in control group were fed with physiological saline by gavage. The trials were conducted for 36 d. At the end of the trials, twenty chicks per group were sacrificed, and the cerebra were collected for measuring the brain indices. Compared with the control group, the activities of total superoxide dismutase (T-SOD) and glutathione peroxidase were significantly decreased in treatment groups (P < 0.05), the contents of malondialdehyde in high dose group were increased (P < 0.05), the catalase activities and nitric oxide contents in medium and high dose groups were decreased (P < 0.05), and the activities of T-AOC in high dose group were reduced (P < 0.05). Compared with the control group, the concentrations of norepinephrine and 5-hydroxytryptamine in high dose group were obviously increased (P < 0.05), while the concentrations of dopamine were decreased (P < 0.05). Meanwhile, the concentrations of calcium and calmodulin (CaM) in medium and high dose groups were lower than those of the control group (P < 0.05), and the gene relative expression of CaM mRNA in treatment groups were significantly reduced (P < 0.05), in a dose-dependent manner. These results suggested that DON exposure can affect the cerebral lipid peroxidation, neurotransmitters secretion and the balance of calcium homeostasis in chicks.

ACS Style

Xichun Wang; Jishun Tang; Fangfang Geng; Lei Zhu; Xiaoyan Chu; Yafei Zhang; Sajid Ur Rahman; Xiaofang Chen; Yunjing Jiang; Dianfeng Zhu; Shibin Feng; Yu Li; Jin Jie Wu. Effects of deoxynivalenol exposure on cerebral lipid peroxidation, neurotransmitter and calcium homeostasis of chicks in vivo. Toxicon 2018, 150, 60 -65.

AMA Style

Xichun Wang, Jishun Tang, Fangfang Geng, Lei Zhu, Xiaoyan Chu, Yafei Zhang, Sajid Ur Rahman, Xiaofang Chen, Yunjing Jiang, Dianfeng Zhu, Shibin Feng, Yu Li, Jin Jie Wu. Effects of deoxynivalenol exposure on cerebral lipid peroxidation, neurotransmitter and calcium homeostasis of chicks in vivo. Toxicon. 2018; 150 ():60-65.

Chicago/Turabian Style

Xichun Wang; Jishun Tang; Fangfang Geng; Lei Zhu; Xiaoyan Chu; Yafei Zhang; Sajid Ur Rahman; Xiaofang Chen; Yunjing Jiang; Dianfeng Zhu; Shibin Feng; Yu Li; Jin Jie Wu. 2018. "Effects of deoxynivalenol exposure on cerebral lipid peroxidation, neurotransmitter and calcium homeostasis of chicks in vivo." Toxicon 150, no. : 60-65.

Research article
Published: 15 April 2018 in Evidence-Based Complementary and Alternative Medicine
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Berberine hydrochloride is an isoquinoline type alkaloid extracted from Berberidaceae, Rutaceae, and other plants. Previous reports have shown that berberine hydrochloride has anti-inflammatory properties. However, the underlying molecular mechanisms remain unclear. In this study, a lipopolysaccharide- (LPS-) induced murine model of mastitis was established to explore the anti-inflammatory action of berberine hydrochloride. Sixty mice that had been lactating for 5–7 days were randomly divided into six groups, including control, LPS, three berberine hydrochloride treatment groups (5, 10, and 20 mg/kg), and a dexamethasone (DEX) (5 mg/kg) group. Berberine hydrochloride was administered intraperitoneally 1 h before and 12 h after LPS-induced mastitis, and all mice were sacrificed 24 h after LPS induction. The pathological and histopathological changes of the mammary glands were observed. The concentrations and mRNA expressions of TNF-α, IL-1β, and IL-6 were measured by ELISA and qRT-PCR. The activation of TLR4 and NF-κB signaling pathways was analyzed by Western blot. Results indicated that berberine hydrochloride significantly attenuated neutrophil infiltration and dose-dependently decreased the secretion and mRNA expressions of TNF-α, IL-1β, and IL-6 within a certain range. Furthermore, berberine hydrochloride suppressed LPS-induced TLR4 and NF-κB p65 activation and the phosphorylation of I-κB. Berberine hydrochloride can provide mice robust protection from LPS-induced mastitis, potentially via the TLR4 and NF-κB pathway.

ACS Style

Xichun Wang; Shibin Feng; Nana Ding; Yanting He; Cheng Li; Manman Li; Xuedong Ding; Hongyan Ding; Jinchun Li; JinJie Wu; Yu Li. Anti-Inflammatory Effects of Berberine Hydrochloride in an LPS-Induced Murine Model of Mastitis. Evidence-Based Complementary and Alternative Medicine 2018, 2018, 1 -9.

AMA Style

Xichun Wang, Shibin Feng, Nana Ding, Yanting He, Cheng Li, Manman Li, Xuedong Ding, Hongyan Ding, Jinchun Li, JinJie Wu, Yu Li. Anti-Inflammatory Effects of Berberine Hydrochloride in an LPS-Induced Murine Model of Mastitis. Evidence-Based Complementary and Alternative Medicine. 2018; 2018 ():1-9.

Chicago/Turabian Style

Xichun Wang; Shibin Feng; Nana Ding; Yanting He; Cheng Li; Manman Li; Xuedong Ding; Hongyan Ding; Jinchun Li; JinJie Wu; Yu Li. 2018. "Anti-Inflammatory Effects of Berberine Hydrochloride in an LPS-Induced Murine Model of Mastitis." Evidence-Based Complementary and Alternative Medicine 2018, no. : 1-9.

Journal article
Published: 01 April 2016 in Environmental Toxicology and Pharmacology
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Deoxynivalenol (DON) has broad toxicity in animals and humans. In this study the impact of DON treatment on apoptotic pathways in PC12 cells was determined. The effects of DON were evaluated on (i) typical indicators of apoptosis, including cellular morphology, cell activity, lactate dehydrogenase (LDH) release, and apoptosis ratio in PC12 cells, and on (ii) the expression of key genes and proteins related to apoptosis, including Bcl-2, Bax, Bid, cytochrome C (Cyt C), apoptosis inducing factor (AIF), cleaved-Caspase9, and cleaved-Caspase3. DON treatment inhibited proliferation of PC12 cells, induced significant morphological changes and apoptosis, promoted the release of Cyt C and AIF from the mitochondria, and increased the activities of cleaved-Caspase9 and cleaved-Caspase3. Bcl-2 expression decreased with increasing DON concentrations, in contrast to Bax and Bid, which were increased with increasing DON concentration. These data demonstrate that DON induces apoptosis in PC12 cells through the mitochondrial apoptosis pathway.

ACS Style

Xichun Wang; Wei Xu; Mengxue Fan; Tingting Meng; Xiaofang Chen; Yunjing Jiang; Dianfeng Zhu; Wenjuan Hu; Jiajie Gong; Shibin Feng; JinJie Wu; Yu Li. Deoxynivalenol induces apoptosis in PC12 cells via the mitochondrial pathway. Environmental Toxicology and Pharmacology 2016, 43, 193 -202.

AMA Style

Xichun Wang, Wei Xu, Mengxue Fan, Tingting Meng, Xiaofang Chen, Yunjing Jiang, Dianfeng Zhu, Wenjuan Hu, Jiajie Gong, Shibin Feng, JinJie Wu, Yu Li. Deoxynivalenol induces apoptosis in PC12 cells via the mitochondrial pathway. Environmental Toxicology and Pharmacology. 2016; 43 ():193-202.

Chicago/Turabian Style

Xichun Wang; Wei Xu; Mengxue Fan; Tingting Meng; Xiaofang Chen; Yunjing Jiang; Dianfeng Zhu; Wenjuan Hu; Jiajie Gong; Shibin Feng; JinJie Wu; Yu Li. 2016. "Deoxynivalenol induces apoptosis in PC12 cells via the mitochondrial pathway." Environmental Toxicology and Pharmacology 43, no. : 193-202.