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紫云英苷通过调节 Treg/Th1 平衡信号通路拮抗镉诱导的鸡肺损伤的作用机制。

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

机构信息

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

Heilongjiang Academy of Agricultural Sciences, Harbin, 150086, China.

出版信息

Ecotoxicol Environ Saf. 2024 Jun 1;277:116364. doi: 10.1016/j.ecoenv.2024.116364. Epub 2024 Apr 23.

Abstract

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-α, and TGF-β, 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.

摘要

本研究旨在探讨 Treg/Th1 失衡在镉诱导的肺损伤中的作用,以及朝蓟素对鸡镉诱导肺损伤的潜在保护作用。镉暴露显著降低了鸡肺组织中的 T-AOC 和 GSH-Px 水平以及 SOD 活性,而 MDA 和 NO 水平则显著升高。这些结果表明镉引发了肺部的氧化应激。组织病理学分析显示,镉暴露进一步诱导了鸡肺中淋巴细胞的浸润,表明镉导致了肺部损伤。进一步分析表明,镉降低了 IL-4 和 IL-10 的表达,但增加了 IL-17、Foxp3、TNF-α和 TGF-β的表达,表明镉暴露诱导了 Treg/Th1 的失衡。此外,镉通过激活 NF-kB 通路并诱导这些通路下游基因(COX-2、iNOS)的表达,从而导致肺组织的炎症损伤,从而对鸡的肺功能产生不良影响。朝蓟素通过增加抗氧化酶的活性和恢复 Treg/Th1 平衡,减轻了镉诱导的鸡肺氧化应激和炎症。综上所述,我们的结果表明,朝蓟素治疗通过恢复 Treg/Th1 平衡,减轻了镉介导的鸡肺损伤的影响。

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