Kim Min-Seok, Han Jin-Young, Kim Sung-Hwan, Jeon Doin, Kim Hyeon-Young, Lee Seung Woong, Rho Mun-Chual, Lee Kyuhong
National Center for Efficacy Evaluation of Respiratory Disease Product, Korea Institute of Toxicology, 30, Baekhak 1-gil, Jeongeup-si, Jeollabuk-do, 56212, Republic of Korea.
National Center for Efficacy Evaluation of Respiratory Disease Product, Korea Institute of Toxicology, 30, Baekhak 1-gil, Jeongeup-si, Jeollabuk-do, 56212, Republic of Korea; Department of Human and Environmental Toxicology, University of Science & Technology, Daejeon, 34113, Republic of Korea.
Respir Physiol Neurobiol. 2018 Jun;252-253:1-9. doi: 10.1016/j.resp.2018.03.001. Epub 2018 Mar 2.
Oleanolic acid acetate (OAA), triterpenoid compound isolated from Vigna angularis (azuki bean), has been revealed anti-inflammatory in several studies. We investigated the effects of OAA against polyhexamethylene guanidine phosphate (PHMG-P)-induced pulmonary inflammation and fibrosis in mice. OAA treatment effectively alleviated PHMG-P-induced lung injury, including the number of total and differential cell in BAL fluid, histopathological lesions and hydroxyproline content in a dose dependent manner. Moreover, OAA treatment significantly decreased the elevations of IL-1β, IL-6, TNF-α, TGF-β1, and fibronectin, and the activation of the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome in the lungs of PHMG-P-treated mice. Cytokines are known to be key modulators in the inflammatory responses that drive progression of fibrosis in injured tissues. The activation of NLRP3 inflammasome has been reported to be involved in induction of inflammatory cytokines. These results indicate that OAA may mitigate the inflammatory response and development of pulmonary fibrosis in the lungs of mice treated with PHMG-P.
从赤小豆中分离得到的三萜类化合物醋酸齐墩果酸（OAA）在多项研究中已显示出抗炎作用。我们研究了OAA对聚六亚甲基胍磷酸盐（PHMG-P）诱导的小鼠肺部炎症和纤维化的影响。OAA治疗有效减轻了PHMG-P诱导的肺损伤，包括支气管肺泡灌洗液中总细胞和不同类型细胞的数量、组织病理学损伤以及羟脯氨酸含量，且呈剂量依赖性。此外，OAA治疗显著降低了PHMG-P处理小鼠肺中白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）、转化生长因子-β1（TGF-β1）和纤连蛋白的升高，以及含吡咯结构域的NOD样受体家族3（NLRP3）炎性小体的激活。已知细胞因子是驱动受损组织纤维化进展的炎症反应中的关键调节因子。据报道，NLRP3炎性小体的激活参与了炎性细胞因子的诱导。这些结果表明，OAA可能减轻PHMG-P处理小鼠肺部的炎症反应和肺纤维化的发展。
