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富含儿茶素的绿茶通过调节BALB/c小鼠的铁死亡来预防颗粒物暴露诱导的心血管细胞毒性。

Green tea enriched with catechins prevents particulate matter exposure-induced cardiovascular cytotoxicity via regulation of ferroptosis in BALB/c mice.

作者信息

Kim Jong Min, Lee Hyo Lim, Go Min Ji, Sung Mi Jeong, Heo Ho Jin

机构信息

Division of Applied Life Science (BK21), Institute of Agriculture and Life Science, Gyeongsang National University, Jinju, 52828 Republic of Korea.

Korea Food Research Institute, Wanju‑gun, 55365 Republic of Korea.

出版信息

Food Sci Biotechnol. 2025 Feb 27;34(10):2255-2267. doi: 10.1007/s10068-025-01831-0. eCollection 2025 Jun.

Abstract

This study was conducted to assess the protective effects of the aqueous green tea extract (GTE) against particulate matter (PM)-induced cardiac dysfunction in BALB/c mice. The GTE treatment ameliorated PM-induced ferroptosis and vascular smooth muscle cells (VSMC) switching in cardiovascular A7r5 cells. The administration of GTE regulated the body weight change, heart index, serum biomarkers, and cardiac antioxidant system. GTE downregulated the inflammatory reaction by inhibiting the protein expression levels of TLR2, TLR4, NOX4, p-Akt, p-JNK, p-IκB-α, Cas-1, iNOS, Ptgs2, HO-1, TNF-α, and IL-1β. In addition, the supplement of GTE ameliorated cardiac damage by regulating the ferroptotic biomarkers such as p53, xCT, GPX4, TFR, and FtH, and mitochondrial apoptosis indicators such as Cas-3, BCl-2, and BAX. It also protected VSMC phenotype levels of SM22α, αSMA, and calponin. This study suggests that GTE might be a potential material to protect PM-induced cardiac damage via ferroptosis and inflammation pathway.

摘要

本研究旨在评估绿茶水提取物(GTE)对BALB/c小鼠颗粒物(PM)诱导的心脏功能障碍的保护作用。GTE处理改善了PM诱导的心血管A7r5细胞中的铁死亡和血管平滑肌细胞(VSMC)转变。GTE的给药调节了体重变化、心脏指数、血清生物标志物和心脏抗氧化系统。GTE通过抑制TLR2、TLR4、NOX4、p-Akt、p-JNK、p-IκB-α、Cas-1、iNOS、Ptgs2、HO-1、TNF-α和IL-1β的蛋白表达水平下调炎症反应。此外,补充GTE通过调节铁死亡生物标志物如p53、xCT、GPX4、TFR和FtH以及线粒体凋亡指标如Cas-3、Bcl-2和BAX改善心脏损伤。它还保护了VSMC的SM22α、αSMA和钙调蛋白的表型水平。本研究表明,GTE可能是一种通过铁死亡和炎症途径保护PM诱导的心脏损伤的潜在物质。

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PM2.5 Exposure and Asthma Development: The Key Role of Oxidative Stress.PM2.5 暴露与哮喘发展:氧化应激的关键作用。
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