EGCG alleviated Mn exposure-caused carp kidney damage via trpm2-NLRP3-TNF-α-JNK pathway: Oxidative stress, inflammation, and tight junction dysfunction

EGCG 通过 trpm2-NLRP3-TNF-α-JNK 通路减轻锰暴露引起的鲤鱼肾脏损伤:氧化应激、炎症和紧密连接功能障碍

阅读:9
作者:Qin Zhou, Jiawen Cui, Yuhang Liu, Lepeng Gu, Xiaohua Teng, You Tang

Abstract

Manganese (Mn), an essential trace metal element in organisms. However, with extensive use of Mn in industry and agriculture, Mn becomes a heavy metal pollutant in water. (-)-epigallocatechin gallate (EGCG), an tea polyphenols, can alleviate metal toxicity. Kidney is an important detoxifying organ, but toxic mechanism of Mn to kidneys is unclear, which needs further research. Carp is an Asian important economical species for fisheries and a biological model for studying environmental toxicology. Thus, we established excess Mn and EGCG-supplemented carp model to explore molecular mechanism of EGCG alleviating Mn-caused carp kidney damage. In this experiment, we set a control group (the Con group), a Mn treatment group (the Mn group, 90 mg/L Mn), a EGCG supplement group (the EG group, 75 mg/kg EGCG), and a combined group (the Mn + EG group, 90 mg/L Mn and 75 mg/kg EGCG). Transcriptome, qRT-PCR, kit, and morphology method results indicated that excess Mn caused oxidative stress, inflammatory damage, and tight junction dysfunction in carp kidneys. Excess Mn-triggered oxidative stress caused tight junction dysfunction via trpm2-NLRP3-TNF-α-JNK pathway and inflammation. EGCG reversed the harm of Mn to fish through the above mechanism. The findings of this study provided the evidence of EGCG-alleviated Mn poisoning and offered new ideas for reducing heavy metal environmental pollution risk.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。