PM2.5inhalation aggravates inflammation, oxidative stress, and apoptosis in nonalcoholic fatty liver disease

• Published in: Environmental disease 2019-07, Vol.4 (3), p.62-68
• Main Authors: Xin, Shen, Qu, Jing, Xu, Na, Xu, Baohong
• Format: Article
• Language: English
• Subjects: Apoptosis; inflammation; nonalcoholic fatty liver disease; oxidative stress
• ISSN: 2468-5690; 2468-5704
• DOI: 10.4103/ed.ed_24_19

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.