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硒通过 PPAR-γ/PI3K/Akt 通路拮抗镉诱导的鸡胰腺细胞凋亡。

The antagonistic effect of selenium on cadmium-induced apoptosis via PPAR-γ/PI3K/Akt pathway in chicken pancreas.

机构信息

College of Veterinary Medicine, Northeast Agricultural University, Harbin, PR China.

College of Veterinary Medicine, Northeast Agricultural University, Harbin, PR China; Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China.

出版信息

J Hazard Mater. 2018 Sep 5;357:355-362. doi: 10.1016/j.jhazmat.2018.06.003. Epub 2018 Jun 1.

DOI:10.1016/j.jhazmat.2018.06.003
PMID:29909169
Abstract

The animal experiment was preformed to investigate the roles of PPAR-γ/PI3K/Akt pathway in apoptosis triggered by cadmium (Cd) and in the antagonistic effects of selenium (Se) on Cd in the pancreas of chicken. The current study showed that Cd treatment obviously increased the accumulation of Cd and directly led to lower activities of amylase, trypsin and lipase in chicken pancreas. The expression of PPAR-γ, PI3K, and Akt was declined, whereas the level of Bax, Cyt C and caspase-3 were increased in Cd group. In the result of TUNEL assay and the histological examination, typical apoptosis characteristics in the pancreas of Cd group were confirmed. Cd group also showed high levels of inducible nitric oxide synthase (iNOS) activity and nitric oxide (NO) content in pancreas. However, those Cd-induced changes were obviously alleviated in Cd + Se group. Our study revealed that Cd could impact the pancreas function and induce the activation of Bax and the overproduction of NO via PPAR-γ/PI3K/Akt pathway to promote apoptosis in chicken pancreas. However, Se could reduce Cd accumulation and antagonize Cd-triggered apoptosis in chicken pancreas.

摘要

本动物实验旨在研究过氧化物酶体增殖物激活受体γ/磷酸肌醇 3-激酶/蛋白激酶 B(PPAR-γ/PI3K/Akt)通路在镉(Cd)诱导的鸡胰腺细胞凋亡中的作用,以及硒(Se)对 Cd 拮抗作用的分子机制。本研究表明,Cd 处理明显增加了 Cd 在鸡胰腺中的蓄积,直接导致淀粉酶、胰蛋白酶和脂肪酶活性降低。Cd 组 PPAR-γ、PI3K 和 Akt 的表达下降,而 Bax、细胞色素 C 和 caspase-3 的水平升高。TUNEL 检测和组织学检查的结果证实了 Cd 组胰腺中出现了典型的凋亡特征。Cd 组胰腺中诱导型一氧化氮合酶(iNOS)活性和一氧化氮(NO)含量也明显升高。然而,Cd+Se 组明显减轻了这些 Cd 诱导的变化。本研究表明,Cd 可能通过 PPAR-γ/PI3K/Akt 通路影响胰腺功能,诱导 Bax 激活和 NO 过度产生,从而促进鸡胰腺细胞凋亡。然而,Se 可以减少 Cd 蓄积,并拮抗 Cd 诱导的鸡胰腺细胞凋亡。

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