Abstract

BACKGROUND: As a member of short-chain fatty acids, acetate exhibits anti-inflammatory capacity. The present study aimed to investigate the effect of acetate on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and explored its underlying mechanism.

MATERIAL AND METHODS: Acetate (250 mM, 400 µL) was given intraperitoneally 30 minutes after LPS (5 mg/kg) intratracheal injection. Lung tissues and bronchoalveolar lavage fluid (BALF) were collected 6 hours after the challenge of LPS. The histopathology scores, wet-to-dry weight ratios, protein content, and cytokine levels in BALF were assessed.

RESULTS: The acetate treatment resulted in improved lung pathological score, alleviated LPS-induced microvascular permeability, and suppressed the production of reactive oxygen species. Furthermore, acetate decreased the level of pro-inflammatory cytokines and chemokines in the lungs and BALF, consistent with the declined immune cell counting found in BALF. In addition, phosphorylation levels of mitogen-activated protein kinase (MAPK) pathway in lung tissues were downregulated by acetate.

CONCLUSIONS: These results suggested that acetate exerts its protective effects via anti-inflammatory and anti-oxidant activities on LPS-induced ALI.

Keywords: acute lung injury, Lipopolysaccharides, mitogen-activated protein kinase, Acetates, Anti-Inflammatory Agents, Bronchoalveolar Lavage Fluid, Cytokines, Injections, Intraperitoneal, Lung, Mice, Inbred C57BL, Mitogen-Activated Protein Kinases, Oxidative Stress, Protective Agents