The antagonism mechanism of astilbin against cadmium-induced injury in chicken lungs via Treg/Th1 balance signaling pathway

文献类型： 外文期刊

第一作者： Shi, Guangliang

作者： Shi, Guangliang;Tai, Tiange;Han, Tianyu;Liu, Zhaoyang;Liu, Yiding;Yang, Yu;Fei, Shanshan;Pang, Bo;Yan, Liangchun;Dong, Han;Cheng, Tingting;Chen, Tiezhu;Shi, Guangliang;Tai, Tiange;Han, Tianyu;Liu, Zhaoyang;Liu, Yiding;Yang, Yu;Fei, Shanshan;Pang, Bo;Chen, Tiezhu;Yan, Liangchun;Dong, Han;Cheng, Tingting;Miao, Yusong

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关键词： Cadmium; Treg/Th1; Oxidative stress; Inflammation; Astilbin

期刊名称：ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY （ 影响因子：6.8； 五年影响因子：6.9 ）

ISSN： 0147-6513

年卷期： 2024 年 277 卷

页码：

收录情况： SCI

摘要： The purpose of this study was to investigate the effect of Treg/Th1 imbalance in cadmium-induced lung injury and the potential protective effect of astilbin against cadmium-induced lung injury in chicken. Cadmium exposure significantly decreased T-AOC and GSH-Px levels and SOD activity in the chicken lung tissues. In contrast, it significantly increased the MDA and NO levels. These results indicate that cadmium triggers oxidative stress in lungs. Histopathological analysis revealed that cadmium exposure further induced infiltration of lymphocytes in the chicken lungs, indicating that cadmium causes pulmonary damage. Further analysis revealed that cadmium decreased the expression of IL -4 and IL -10 but increased those of IL -17, Foxp3, TNF- alpha, and TGF- beta , indicating that the exposure of cadmium induced the imbalance of Treg/Th1. Moreover, cadmium adversely affected chicken lung function by activating the NF-kB pathway and inducing expression of genes downstream to these pathways (COX -2, iNOS), associated with inflammatory injury in the lung tissue. Astilbin reduced cadmium-induced oxidative stress and inflammation in the lungs by increasing antioxidant enzyme activities and restoring Treg/Th1 balance. In conclusion, our results suggest that astilbin treatment alleviated the effects of cadmium-mediated lung injury in chickens by restoring the Treg/Th1 balance.

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