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Liu J.,Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province | Cui H.,Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province | Cui H.,Sichuan Agricultural University | Peng X.,Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province | And 8 more authors.
Fluoride | Year: 2012

As part of our recent studies on the effects of high fluorine (F) on the cecal tonsil of newly hatched chickens, the same broilers with 400, 800, and 1200 mg F/kg in their diet were used to investigate the changes in the cecal tonsil content of the cytokine proteins interleukin-4 (IL-4), interleukin-6 (IL-6), tumour necrosis factor alpha (TNF-α), and interferon gamma (IFN-γ) by enzyme-linked immunosorbent assay (ELISA). The results showed that the content of these cytokines in the cecal tonsil was significantly lower (p<0.05 or p<0.01) in the high F groups II and III than in the control group. Lower cytokine levels in the cecal tonsil can impact the local immune function of intestines by affecting pathways that decrease the lymphocyte numbers and/or lymphocyte activation. © 2012 The International Society for Fluoride Research Inc.


Guo H.,Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province | Cui H.,Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province | Cui H.,Sichuan Agricultural University | Peng X.,Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province | And 11 more authors.
Oncotarget | Year: 2015

Here we showed that dietary NiCl2 in excess of 300 mg/kg caused the G2/M cell cycle arrest and the reduction of cell proportion at S phase. The G2/M cell cycle arrest was accompanied by up-regulation of phosphorylated ataxia telangiectasia mutated (p-ATM), p53, p-Chk1, p-Chk2, p21 protein expression and ATM, p53, p21, Chk1, Chk2 mRNA expression, and down-regulation of p-cdc25C, cdc2, cyclinB and proliferating cell nuclear antigen (PCNA) protein expression and the cdc25, cdc2, cyclinB, PCNA mRNA expression.


PubMed | Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province and Sichuan Agricultural University
Type: | Journal: Chemico-biological interactions | Year: 2015

The aims of this study were to investigate the pathways which dietary nickel chloride (NiCl2) affects small intestine apoptosis in broiler chickens by observing the ultrastructure, and bcl-2, bax, and caspase-3 protein expression and mRNA expression, and cytochrome C, bak and caspase-9 mRNA expression of the small intestine. A total of 240 one-day-old avian broilers were divided into four groups and fed a corn-soybean basal diet as the control diet or three experimental diets supplemented with 300, 600, and 900mg/kg of NiCl2 for 42 days. Ultrastructurally, the microvilli were apparently exfoliated, and the mitochondria were swollen and the number of lysosomes increased in the intestinal cells of three experimental groups. As measured by TUNEL and flow cytometry (FCM), the percentage of apoptotic cells in the small intestine and the lymphocytes in the ileum were significantly increased in three experimental groups when compared with those of the control group. Meanwhile, immunohistochemistry, quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immuno-sorbent assay (ELISA) tests showed that the protein expression, mRNA expression levels were decreased in the bcl-2, whereas those of bax and caspase-3, and the cytochrome C, bak and caspase-9 mRNA expression levels were increased in three experimental groups. The abovementioned results show that pathway of dietary NiCl2-induced small intestine apoptosis is related to the mitochondrial damage and promotion of the cytochrome C release from mitochondria, which activates the mitochondrion-mediated apoptosis pathway.


PubMed | Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province and Sichuan Agricultural University
Type: | Journal: Ecotoxicology and environmental safety | Year: 2014

This study was designed to evaluate the toxicological effect of dietary nickel chloride (NiCl2) on the counts of intestinal bacteria and diversity of microorganisms in broilers. Plate counting and polymerase chain reaction-denaturing gradient gel electrophoresis (PCR-DGGE) assays were used. A total of 240 one-day-old avian broilers chicks were divided into four equal groups and kept on corn-soybean basal diet along with supplementation of 0, 300, 600 and 900 mg/kg NiCl2 for 42 days. Samples were taken at 21 and 42 days of age during the experiment. The bacterial count results showed that dietary NiCl2 in the range of 300 to 900 mg/kg decreased the counts of Bifidobacterium spp. and Lactobacillus, increased Escherichia coli (E. coli) and Enterococcus spp. in the ileum and cecum. PCR-DGGE analysis showed that bacterial band numbers, profile similarity, and the Shannon index of the ileum and cecum were all decreased in the 300, 600, and 900 mg/kg groups at 21 and 42 days of age. In conclusion, dietary NiCl2 affected the amount and diversity of intestinal microbiota in the ileum and cecum of broilers. This finding implies that NiCl2 has toxicological effect on the intestinal ecosystem and, possibly functions.


PubMed | Tongren University, Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province and Sichuan Agricultural University
Type: Journal Article | Journal: Oncotarget | Year: 2016

Aflatoxin B1 (AFB1) has potent hepatotoxic, carcinogenic, genotoxic, immunotoxic and other adverse effects in human and animals. The aim of this study was to investigate the molecular mechanism of G2/M cell cycle arrest induced by AFB1 in the jejunum of broilers. Broilers, as experimental animals, were fed 0.6 mg/kg AFB1 diet for 3 weeks. Our results showed that AFB1 reduced the jejunal villus height, villus height/crypt ratio and caused G2/M cell cycle arrest. The G2/M cell cycle was accompanied by the increase of ataxia telangiectasia mutated (ATM), p53, Chk2, p21 protein and mRNA expression, and the decrease of Mdm2, cdc25C, cdc2, cyclin B and proliferating cell nuclear antigen protein and mRNA expression. In conclusion, AFB1 blocked G2/M cell cycle by ATM pathway in the jejunum of broilers.


PubMed | Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province and Sichuan Agricultural University
Type: Journal Article | Journal: International journal of molecular sciences | Year: 2015

This study was conducted to investigate the effects of aflatoxin B1 (AFB1) on T-cell subsets and mRNA expression of cytokines in the small intestine of broilers. One hundred and fifty-six one-day-old healthy Cobb broilers were randomly divided into control group (0 mg/kg AFB1) and AFB1 group (0.6 mg/kg AFB1) with three replicates per group and 26 birds per replicate for 21 days, respectively. At 7, 14, and 21 days of age, the duodenum, jejunum and ileum were sampled for analyzing T cell subsets (CD3+, CD3+CD4+ and CD3+CD8+) by flow cytometry as well as IL-2, IL-4, IL-6, IL-10, IL-17, IFN- and TNF- mRNA expression by qRT-PCR. The percentages of T-cells in the intra-epithelial lymphocytes (IELs) and lamina propria lymphocytes (LPLs) of duodenum, jejunum and ileum in the AFB1 group showed a decreased tendency in comparison to the control group. The mRNA expression of cytokines in the three intestinal segments in the AFB1 group presented a general decline compared with the control groups. Our data demonstrated that 0.6 mg/kg AFB1 in the broilers diet could reduce the percentages of T-cell subsets and the expression level of cytokine mRNA in the small intestine, implying that the immune function of the intestinal mucosa might be affected. The reduction of cytokines mRNA expression may be closely associated with the decreased proportions of T cells subsets induced by AFB1.


PubMed | Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province
Type: Journal Article | Journal: Oncotarget | Year: 2015

Here we showed that dietary NiCl2 in excess of 300 mg/kg caused the G2/M cell cycle arrest and the reduction of cell proportion at S phase. The G2/M cell cycle arrest was accompanied by up-regulation of phosphorylated ataxia telangiectasia mutated (p-ATM), p53, p-Chk1, p-Chk2, p21 protein expression and ATM, p53, p21, Chk1, Chk2 mRNA expression, and down-regulation of p-cdc25C, cdc2, cyclinB and proliferating cell nuclear antigen (PCNA) protein expression and the cdc25, cdc2, cyclinB, PCNA mRNA expression.

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