Lee Jae-Won, Park Hyun Ah, Kwon Ok-Kyoung, Jang Yin-Gi, Kim Ju Yeong, Choi Bo Kyung, Lee Hee Jae, Lee Sangwoo, Paik Jin-Hyub, Oh Sei-Ryang, Ahn Kyung-Seop, Lee Hyun-Jun
Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, 30 Yeongudanji-ro, Ochang-eup, Cheongwon-gu, Chungju-si, Chungbuk 363-883, Republic of Korea.
Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, 30 Yeongudanji-ro, Ochang-eup, Cheongwon-gu, Chungju-si, Chungbuk 363-883, Republic of Korea; College of Pharmacy, Chungnam National University, 99 Daehak-ro, Yuseong-gu, Daejeon 305-764, Republic of Korea.
Int Immunopharmacol. 2016 Oct;39:208-217. doi: 10.1016/j.intimp.2016.07.010. Epub 2016 Aug 3.
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.
积雪草苷(AA)是积雪草滴定提取物(TECA)的主要成分之一,据报道其具有抗氧化和抗炎活性。本研究的目的是探讨AA对香烟烟雾(CS)诱导的肺部炎症的保护作用。AA显著减轻了CS暴露小鼠支气管肺泡灌洗液(BALF)中炎症细胞的浸润。AA还降低了活性氧的产生和中性粒细胞弹性蛋白酶(NE)的活性,并抑制了BALF中促炎细胞因子的释放。AA减少了CS暴露小鼠肺组织中炎症细胞的募集和单核细胞趋化蛋白-1(MCP-1)的表达。AA还减轻了黏液过度分泌,并降低了肺组织中丝裂原活化蛋白激酶(MAPKs)和核因子κB(NF-κB)的活化。此外,AA增加了肺组织中血红素加氧酶-1(HO-1)的表达,并抑制了超氧化物歧化酶3(SOD3)表达的降低。这些发现表明,AA通过抑制炎症介质和诱导HO-1,有效抑制了肺部炎症反应,而肺部炎症反应是慢性阻塞性肺疾病(COPD)发展过程中的一个重要过程。因此,我们认为AA具有治疗COPD等炎症性疾病的潜力。