Asiatic acid inhibits pulmonary inflammation induced by cigarette smoke

• Asiatic acid (AA) is a well-known herbal medicine in China.
• AA attenuates neutrophil recruitment and mucus overproduction in lung of CS exposure mice.
• AA decreases the inflammatory mediators and suppresses the activation of MAPKs and NF-kB.
• AA increases HO-1 expression and inhibits the reduced expression of SOD3.
• AA may be a valuable therapeutics in the treatment of COPD.

Asiatic acid (AA) is one of the major components of Titrated extract of Centella asiatica (TECA), which has been reported to possess antioxidant and anti-inflammatory activities. The purpose of this study was to investigate the protective effect of AA on pulmonary inflammation induced by cigarette smoke (CS). AA significantly attenuated the infiltration of inflammatory cells in bronchoalveolar lavage fluid (BALF) of CS exposure mice. AA also decreased ROS production and NE activity, and inhibited the release of proinflammatory cytokines in BALF. AA reduced the recruitment of inflammatory cells and MCP-1 expression in lung tissue of CS exposure mice. AA also attenuated mucus overproduction, and decreased the activation of MAPKs and NF-kB in lung tissue. Furthermore, AA increased HO-1 expression and inhibited the reduced expression of SOD3 in lung tissue. These findings indicate that AA effectively inhibits pulmonary inflammatory response, which is an important process in the development of chronic obstructive pulmonary disease (COPD) via suppression of inflammatory mediators and induction of HO-1. Therefore, we suggest that AA has the potential to treat inflammatory disease such as COPD.

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