Ganoderic Acid B Attenuates Lps-Induced Lung Injury

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a serious respiratory disease, the mechanism is unclear. This paper revealed the mechanism of ganoderic acid B (BB) on lipopolysaccharide-induced pneumonia in mice. Pneumonia model was induced by LPS in mice and A549 cells. Lung dry/wet weight (W/D) and myeloperoxidase (MPO) activity in lung were examined. Lung histopathological changes was observed by HE staining. Superoxide dismutase (SOD), malondialdehyde (MDA) and proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) in mice and A549 cells were detected. Rho/NF-kappa B pathway in mice and A549 cells were examined by Western Blot. BB significantly reduced W/D and MPO activity, restored lung histopathological changes. BB also increased SOD, decreased MDA, TNF-alpha, IL-1 beta and IL-6 in mice and A549 cells. In addition, BB inhibited Rho/NF-kappa B pathway in mice and A549 cells. BB has protective effect on LPS-induced pneumonia in mice, and its mechanism is related to the regulation of Rho/NF-kappa B signaling pathway.