Liou Chian-Jiun, Lai You-Rong, Chen Ya-Ling, Chang Yi-Hsien, Li Zih-Ying, Huang Wen-Chung
Department of Nursing, Chang Gung University of Science and Technology, No. 261 Wenhua 1st Road, Guishan District, Taoyuan City 33303, Taiwan; Chang Gung Memorial Hospital at Linkou, Guishan District, Taoyuan City 33303, Taiwan.
Department of Nutrition and Health Sciences, Chang Gung University of Science and Technology, No. 261 Wenhua 1st Road, Guishan District, Taoyuan City 33303, Taiwan.
Mediators Inflamm. 2016;2016:3630485. doi: 10.1155/2016/3630485. Epub 2016 Jan 5.
Matrine is isolated from Sophora flavescens and shows anti-inflammatory effects in macrophages. Here we evaluated matrine's suppressive effects on cyclooxygenase 2 (COX-2) and intercellular adhesion molecule-1 (ICAM-1) expressions in lipopolysaccharide- (LPS-) stimulated human lung epithelial A549 cells. Additionally, BALB/c mice were given various matrine doses by intraperitoneal injection, and then lung injury was induced via intratracheal instillation of LPS. In LPS-stimulated A549 cells, matrine inhibited the productions of interleukin-8 (IL-8), monocyte chemotactic protein-1, and IL-6 and decreased COX-2 expression. Matrine treatment also decreased ICAM-1 protein expression and suppressed the adhesion of neutrophil-like cells to inflammatory A549 cells. In vitro results demonstrated that matrine significantly inhibited mitogen-activated protein kinase phosphorylation and decreased nuclear transcription factor kappa-B subunit p65 protein translocation into the nucleus. In vivo data indicated that matrine significantly inhibited neutrophil infiltration and suppressed productions of tumor necrosis factor-α and IL-6 in mouse bronchoalveolar lavage fluid and serum. Analysis of lung tissue showed that matrine decreased the gene expression of proinflammatory cytokines, chemokines, COX-2, and ICAM-1. Our findings suggest that matrine improved lung injury in mice and decreased the inflammatory response in human lung epithelial cells.
苦参碱是从苦参中分离出来的,在巨噬细胞中显示出抗炎作用。在此,我们评估了苦参碱对脂多糖(LPS)刺激的人肺上皮A549细胞中环氧合酶2(COX-2)和细胞间黏附分子1(ICAM-1)表达的抑制作用。此外,通过腹腔注射给予BALB/c小鼠不同剂量的苦参碱,然后通过气管内滴注LPS诱导肺损伤。在LPS刺激的A549细胞中,苦参碱抑制白细胞介素-8(IL-8)、单核细胞趋化蛋白-1和IL-6的产生,并降低COX-2表达。苦参碱处理还降低了ICAM-1蛋白表达,并抑制了中性粒细胞样细胞与炎性A549细胞的黏附。体外结果表明,苦参碱显著抑制丝裂原活化蛋白激酶磷酸化,并减少核转录因子κB亚基p65蛋白向细胞核的转位。体内数据表明,苦参碱显著抑制小鼠支气管肺泡灌洗液和血清中中性粒细胞浸润,并抑制肿瘤坏死因子-α和IL-6的产生。肺组织分析表明,苦参碱降低了促炎细胞因子、趋化因子、COX-2和ICAM-1的基因表达。我们的研究结果表明,苦参碱改善了小鼠的肺损伤,并降低了人肺上皮细胞中的炎症反应。