Effects of Ergosterol, Isolated from Scleroderma Polyrhizum Pers., on Lipopolysaccharide-Induced Inflammatory Responses in Acute Lung Injury

• Published in: Inflammation 2015-10, Vol.38 (5), p.1979-1985
• Main Authors: Zhang, Shu-ying, Xu, Li-ting, Li, Ai-xin, Wang, Shu-min
• Format: Article
• Language: English
• Subjects: Acute Lung Injury - chemically induced; Acute Lung Injury - drug therapy; Acute Lung Injury - metabolism; Animals; Anti-Inflammatory Agents - isolation & purification; Anti-Inflammatory Agents - therapeutic use; Biomedical and Life Sciences; Biomedicine; Ergosterol - isolation & purification; Ergosterol - therapeutic use; Female; Fungi; Immunology; Internal Medicine; Lipopolysaccharides - toxicity; Mice; Mice, Inbred BALB C; Pathology; Pharmacology/Toxicology; Rheumatology
• ISSN: 0360-3997; 1573-2576
• DOI: 10.1007/s10753-015-0178-1

The present study aimed to investigate the protective role of ergosterol, isolated from Scleroderma polyrhizum Pers., in lipopolysaccharide (LPS)-induced acute lung injury (ALI). ALI was induced in mice by LPS (0.5 mg/kg), and ergosterol (25 and 50 mg/kg) was administrated orally 1 h prior to LPS administration. Ergosterol pretreatment at doses of 25 and 50 mg/kg decreased LPS-induced lung histopathological changes, lung wet-to-dry weight ratio. In addition, pretreatment with ergosterol inhibited inflammatory cells and proinflammatory cytokines including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Furthermore, we demonstrated that ergosterol blocked the activation of nuclear factor-kappaB (NF-κB), cyclooxygenase (COX)-2, and nitric oxide synthase (iNOS) pathways. The results presented here suggest that the protective mechanism of ergosterol may be attributed partly to the inhibition of NF-κB, COX-2, and iNOS pathways.