摘要
目的对从山葡萄籽来源的山葡萄素A和二脱氢山葡萄素A发挥抗动脉粥样硬化作用的分子机制进行深入的研究。方法采用体外培养的人脐静脉内皮细胞Hy926、鼠巨噬细胞RAM264.7和佛波酯(PMA)诱导的人单核细胞源性巨噬细胞THP-1,加入氧化低密度脂蛋白(ox-LDL)和脂多糖(LPS)损伤后,通过检测细胞活力(MTT法和LDH法)、活性氧、一氧化氮、丙二醛(MDA)和超氧化物歧化酶(SOD)的含量,以及细胞上清中细胞因子肿瘤坏死因子(TNF-α)和白介素1β(IL-1β)的分泌,单核细胞THP-1和内皮细胞Hy926的黏附作用,考察化合物的作用。结果化合物对ox-LDL导致的内皮细胞和巨噬细胞损伤有较明显的保护作用,并且抗氧化,减少氧、氮自由基产生,抑制LPS所致的巨噬细胞炎性因子释放,抑制单核细胞和内皮细胞黏附。结论山葡萄素A和二脱氢山葡萄素A对动脉粥样硬化(atherosclerosis,AS)发生早期事件的多个关键环节均有作用,提示其可能的动脉粥样硬化保护分子机制涉及多个靶点和通路的相互作用。
Aim To elucidate the anti-atherosclerotic mechanism of vitisinA and didehydro-vitisinA from Vitis amurensis.Methods After the human endothelial cell Hy926,monocyte derived THP-1 macrophage and mouse macrophage RAW264.7 were damaged by oxLDL and LPS in vitro,the effects of the two test compounds were observed on cell viability by MTT reduction and LDH activity assay,the release of ROS and NO,the content of MDA,the activity of SOD,the secretion of inflammatory cytokines TNF-α and IL-1β,and the cell adhesion of THP-1 monocyte and endothelial cell Hy926.Results The two compounds produced marked effects on protecting cells from injury,reducing the production of free radicals and the secretion of inflammatory cytokines,antioxcidation,and inhibiting the cell adhesion of monocyte and endothelial cells.Conclusions It is observed that vitisinA and didehydro-vitisinA can regulate factors which were important in the initiation and early progression of atherosclerosis,and their possible anti-atherosclerosis mechanism may be involved in multiple pathways.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2010年第9期1192-1198,共7页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助项目(No30901976)
