吸入pm2.5可加重非酒精性脂肪肝患者的炎症、氧化应激和细胞凋亡

Shen Xin, Jingjing Qu, Na Xu, Baohong Xu
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引用次数: 1

摘要

背景:2.5 μm以下的颗粒物(PM2.5)是非酒精性脂肪性肝病(NAFLD)的主要危险因素。本研究旨在探讨pm2.5是否会加重NAFLD及其相关机制。材料与方法:雄性Sprague-Dawley大鼠分别暴露于pm2.5和过滤空气中4、6、8周。采用酶联免疫吸附试验(ELISA)测定血脂。苏木精染色、伊红染色观察肝脏组织病理学变化。采用ELISA法检测炎症标志物,包括白细胞介素-17 (IL-17)或肿瘤坏死因子α (TNF-α),并评估氧化应激相关蛋白,包括超氧化物歧化酶(SOD)和丙二醛(MDA)。通过实时聚合酶链反应和Western blotting检测b细胞淋巴瘤-2 (Bcl-2)和Bcl-2相关X蛋白(BAX)来评估细胞凋亡。结果:pm2.5暴露8周,而不是4周和6周,NAFLD明显加重,与IL-17和TNF-α表达增加以及氧化应激(SOD和MDA)增加有关。同时,暴露于pm2.5 8周,而不是4周或6周,细胞凋亡(Bcl-2和BAX)受到调节。结论:pm2.5暴露8周可加重NAFLD,其可能通过肝脏炎症、氧化应激和细胞凋亡介导。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
PM2.5inhalation aggravates inflammation, oxidative stress, and apoptosis in nonalcoholic fatty liver disease
Background: Particulate matter under 2.5 μm (PM2.5) is a major risk factor for nonalcoholic fatty liver disease (NAFLD). This study aimed to investigate whether PM2.5could aggravate NAFLD, as well as its relative mechanisms. Materials and Methods: Male Sprague-Dawley rats were under PM2.5exposure and filtered air with NAFLD for 4, 6, and 8 weeks. Blood lipids were measured by enzyme-linked immunosorbent assay (ELISA). The histopathology of liver was determined by hematoxylin and eosin staining. ELISA assay was conducted for detecting inflammatory markers including interleukin-17 (IL-17) or tumor necrosis factor alpha (TNF-α) and for assessing oxidative stress-associated proteins, including superoxide dismutase (SOD) and malondialdehyde (MDA). Apoptosis was assessed by detecting B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (BAX) by real-time polymerase chain reaction and Western blotting. Results: PM2.5exposure for 8 weeks, but not 4 or 6 weeks, significantly aggravated NAFLD, which was associated with the enhanced expression of IL-17 and TNF-α and the enhanced oxidative stress (SOD and MDA). Meanwhile, exposure PM2.5for 8 weeks, but not 4 or 6 weeks, regulated apoptosis (Bcl-2 and BAX). Conclusions: Exposure of PM2.5for 8 weeks can aggravate NAFLD, which may be mediated by liver inflammation, oxidative stress, and apoptosis.
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