Selenium Ameliorates AFB1−Induced Excess Apoptosis in Chicken Splenocytes Through Death Receptor and Endoplasmic Reticulum Pathways
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Aflatoxin B1 (AFB1) can cause hepatotoxicity, genotoxicity, and immunosuppressive effects for a variety of organisms. Selenium (Se), as an essential nutrient element, plays important protective effects against cell apoptosis induced by AFB1. This research aimed to reveal the ameliorative effects of selenium on AFB1-induced excess apoptosis in chicken splenocytes through death receptor and endoplasmic reticulum pathways in vivo. Two hundred sixteen neonatal chickens, randomized into four treatments, were fed with basal diet (control treatment), 0.4 mg/kg Se supplement (+Se treatment), 0.6 mg/kg AFB1 (AFB1 treatment), and 0.6 mg/kg AFB1 + 0.4 mg/kg Se (AFB1 + Se treatment) during 21 days of experiment, respectively. Compared with the AFB1 treatment, the levels of splenocyte apoptosis in the AFB1 + Se treatment were obviously dropped by flow cytometry and TUNEL assays although they were still significantly higher than those in the control or + Se treatments. Furthermore, the mRNA expressions of CASP-3, CASP-8 and CASP-10, GRP78, GRP94, TNF-α, TNF-R1, FAS, and FASL of splenocytes in the AFB1 + Se treatment by qRT-PCR assay were significantly decreased compared with the AFB1 treatment. These results indicate that Se could partially ameliorate the AFB1-caused excessive apoptosis of chicken splenocytes through downregulation of endoplasmic reticulum and death receptor pathway molecules. This research may rich the knowledge of the detoxification mechanism of Se on AFB1-induced apoptosis.
KeywordsSodium selenite AFB1 Splenocyte apoptosis Endoplasmic reticulum molecules Death receptor molecules Chicken
This work was supported by the program for Changjiang scholars, the University Innovative Research Team (IRT 0848), the Education Department of Sichuan Province (2012FZ0066) and (2013FZ0072) and Huimin project of Chengdu science and technology (2016-HM01-00337-SF).
Compliance with Ethical Standards
Conflict of Interest
The authors declare that they have no conflicts of interest.
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