Entity

Time filter

Source Type


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. Source


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 9 more authors.
Fluoride | Year: 2012

As part of our study on the effect of high fluorine (F) on cecal tonsil, changes in the percentages of subsets and IL-2 contents in the cecal tonsil T-cells were investigated in broilers fed high F diets containing 400, 800, and 1200 mg F/kg. The percentages of CD3+, CD3+CD4+, and CD3+CD8+ T-cells in the cecal tonsil were significantly decreased (p<0.05 or p<0.01) in high F groups II and III; however, the CD4+/CD8+ ratio was not significantly changed. Meanwhile, interleukin-2 (IL-2) contents in the cecal tonsil were also lower (p<0.05 or p<0.01) in high F groups II and III than those in the control group. In conclusion, dietary F in the range of 800~1200 mg/kg reduced the percentages of cecal tonsil T-cell subsets and IL-2 contents, implying that the local mucosal immune function can be adversely impacted by high F in broilers. © 2012 The International Society for Fluoride Research Inc. Source


Yin H.,Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province | Jiang M.,Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province | Peng X.,Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province | Peng X.,Sichuan Agricultural University | And 10 more authors.
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. Source


Wu B.,Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province | 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 | And 10 more authors.
Chemico-Biological Interactions | Year: 2016

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 900 mg/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. © 2015 Elsevier Ireland Ltd.All rights reserved. Source


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: 2016

It has been known that overexposure to Ni can induce nephrotoxicity. However, the mechanisms of underlying Ni nephrotoxicity are still elusive, and also Ni- and Ni compound-induced ER stress has been not reported in vivo at present. Our aim was to use broiler chickens as animal model to test whether the ER stress was induced and UPR was activated by NiCl2 in the kidney using histopathology, immunohistochemistry and qRT-PCR. Two hundred and eighty one-day-old broiler chickens were divided into 4 groups and fed on a control diet and the same basal diet supplemented with 300 mg/kg, 600mg/kg and 900mg/kg of NiCl2 for 42 days. We found that dietary NiCl2 in excess of 300 mg/kg induced ER stress, which was characterized by increasing protein and mRNA expression of ER stress markers, e.g., GRP78 and GRP94. Concurrently, all the three UPR pathways were activated by dietary NiCl2. Firstly, the PERK pathway was activated by increasing eIF2a and ATF4 mRNA expression. Secondly, the IRE1 pathway was activated duo to increase in IRE1 and XBP1 mRNA expression. And thirdly, the increase of ATF6 mRNA expression suggested that ATF6 pathway was activated. The findings clearly demonstrate that NiCl2 induces the ER stress through activating PERK, IRE1 and ATF6 UPR pathways, which is proved to be a kind of molecular mechanism of Ni- or/and Ni compound-induced nephrotoxicity. Source

Discover hidden collaborations