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Abstract Title:

Asiatic acid inhibits pulmonary inflammation induced by cigarette smoke.

Abstract Source:

Int Immunopharmacol. 2016 Oct ;39:208-217. Epub 2016 Aug 3. PMID: 27494684

Abstract Author(s):

Jae-Won Lee, Hyun Ah Park, Ok-Kyoung Kwon, Yin-Gi Jang, Ju Yeong Kim, Bo Kyung Choi, Hee Jae Lee, Sangwoo Lee, Jin-Hyub Paik, Sei-Ryang Oh, Kyung-Seop Ahn, Hyun-Jun Lee

Article Affiliation:

Jae-Won Lee

Abstract:

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.

Study Type : Animal Study

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