Selenium Ameliorates AFB1-Induced Excess Apoptosis in Chicken Splenocytes Through Death Receptor and Endoplasmic Reticulum Pathways.

Selenium Ameliorates AFB1-Induced Excess Apoptosis in Chicken Splenocytes Through Death Receptor and Endoplasmic Reticulum Pathways. Biol Trace Elem Res. 2018 May 16;: Authors: Fang J, Zhu P, Yang Z, Peng X, Zuo Z, Cui H, Ouyang P, Shu G, Chen Z, Huang C, Liu W Abstract 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 decr...
Source: Biological Trace Element Research - Category: Biology Authors: Tags: Biol Trace Elem Res Source Type: research