Dahae Lim1, Euijeong Lee1, Eunyoung Jeong2, Young-Pyo Jang2, Jinju Kim3. 1. Department of Korean Physiology, College of Pharmacy, Kyung Hee University, Seoul, Republic of Korea. 2. Department of Life and Nanopharmaceutical Sciences, College of Pharmacy, Kyung Hee University, Seoul, Republic of Korea. 3. Department of Korean Physiology, College of Pharmacy, Kyung Hee University, Seoul, Republic of Korea. Electronic address: shdwer@khu.ac.kr.
Abstract
ETHNOPHARMACOLOGICAL RELEVANCE: Stemona tuberosa (ST) is a traditional herbal medicine used for the treatment of various respiratory diseases in eastern Asia. AIM OF THE STUDY: We investigated the anti-inflammatory effects of a ST water extract in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages and in cigarette smoke (CS)-induced lung inflammation mouse models. MATERIALS AND METHODS: RAW 264.7 macrophages were treated with the ST extract and stimulated by LPS. The expressions of pro-inflammatory mediators were evaluated by using nitric oxide (NO) assay, enzyme-linked immunosorbent assay and Western blot analysis. After the C57BL/6 mice were exposed to CS, they were administrated with the ST extract. The accumulated inflammatory cells in the bronchoalveolar lavage fluid (BALF) were counted. Also, real-time polymerase chain reaction and hematoxylin and eosin staining were performed in lung tissues. RESULTS: The ST extract treatment reduced the production of NO via blocking the expressions of cyclooxygenase-2 and inducible nitric oxide synthase protein in RAW 264.7 macrophages. In addition, ST extract treatment decreased the secretions of inflammatory cytokines and regulated NF-κB activation by inhibiting the phosphorylation of IκB and the mitogen-activated protein kinase pathway. Also, ST extract administration to mice reduced the infiltrations of macrophages into BALF and the histological inflammatory changes in lung tissues. Furthermore, administration of the ST extract regulated the levels of tumor necrosis factor-α, interleukin (IL)-6, IL-1β, monocyte chemoattractant protein-1 and matrix metalloproteinases-12 in the lungs. CONCLUSION: These findings suggested that ST extract attenuated pulmonary inflammatory responses by inhibiting the expression of diverse inflammatory mediators in vivo and in vitro.
ETHNOPHARMACOLOGICAL RELEVANCE: Stemona tuberosa (ST) is a traditional herbal medicine used for the treatment of various respiratory diseases in eastern Asia. AIM OF THE STUDY: We investigated the anti-inflammatory effects of a STwater extract in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages and in cigarette smoke (CS)-induced lung inflammationmouse models. MATERIALS AND METHODS: RAW 264.7 macrophages were treated with the ST extract and stimulated by LPS. The expressions of pro-inflammatory mediators were evaluated by using nitric oxide (NO) assay, enzyme-linked immunosorbent assay and Western blot analysis. After the C57BL/6 mice were exposed to CS, they were administrated with the ST extract. The accumulated inflammatory cells in the bronchoalveolar lavage fluid (BALF) were counted. Also, real-time polymerase chain reaction and hematoxylin and eosin staining were performed in lung tissues. RESULTS: The ST extract treatment reduced the production of NO via blocking the expressions of cyclooxygenase-2 and inducible nitric oxide synthase protein in RAW 264.7 macrophages. In addition, ST extract treatment decreased the secretions of inflammatory cytokines and regulated NF-κB activation by inhibiting the phosphorylation of IκB and the mitogen-activated protein kinase pathway. Also, ST extract administration to mice reduced the infiltrations of macrophages into BALF and the histological inflammatory changes in lung tissues. Furthermore, administration of the ST extract regulated the levels of tumor necrosis factor-α, interleukin (IL)-6, IL-1β, monocyte chemoattractant protein-1 and matrix metalloproteinases-12 in the lungs. CONCLUSION: These findings suggested that ST extract attenuated pulmonary inflammatory responses by inhibiting the expression of diverse inflammatory mediators in vivo and in vitro.