| ORIGINAL ARTICLE |
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| Year : 2019 | Volume
: 4
| Issue : 3 | Page : 62-68 |
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PM2.5inhalation aggravates inflammation, oxidative stress, and apoptosis in nonalcoholic fatty liver disease
Shen Xin1, Jing Qu2, Na Xu2, Baohong Xu1
1 Department of Gastroenterology, Beijing Luhe Hospital, Capital Medical University, Beijing, China
2 Department of Geriatric Medicine, Beijing Luhe Hospital, Capital Medical University, Beijing, China
Correspondence Address:
Dr. Baohong Xu
Department of Gastroenterology, Beijing Luhe Hospital, Capital Medical University, Beijing 101149
China
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ed.ed_24_19
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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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