摘要
目的:研究伪原薯蓣皂苷对氧化低密度脂蛋白(OX-LDL)诱导人血管平滑肌细胞环氧合酶-2(COX-2)表达的影响及机制。方法:培养人冠状动脉平滑肌细胞(HCASMC),加入伪原薯蓣皂苷预处理细胞24小时,加入OX-LDL诱导COX-2表达,采用RT-q PCR和Western blot方法分别检测COX-2的m RNA和蛋白表达水平,检测了与COX-2炎症信号通路相关的激酶活性。结果:伪原薯蓣皂苷(60、30、15μg/ml)为有效剂量,可显著降低OX-LDL诱导的COX-2表达,呈现剂量依赖。伪原薯蓣皂苷(60、30、15μg/ml)也明显抑制与COX-2表达相关的TLR2表达和p38MAPK等激酶活性。结论:伪原薯蓣皂苷通过影响TLR2/p38MAPK通路而抑制下游炎症介质COX-2表达,可能是抑制OX-LDL引起的平滑肌细胞炎性损伤的机制。
Objective： To investigate the effect of pseudoprotodioscin on cyclooxygenase-2 （COX-2） expression induced by OX-LDL in human coro- nary artery vascular smooth muscle cells （HCASMC） and the mechanism. Methods： Human HCASMC cells were cultured in vitro, after pre- treatment with and different concentrations of pseudoprotodiosein for 24 h, OX-LDL was added for the induction of COX-2 expression. The ex- pressions of COX-2 mRNA was detected by RT-qPCR, and the expression of COX-2 protein and the phosphorylation of mitogen activated pro- tein kinase （MAPK） associated with COX-2 inflammatory signaling pathway were detected by Western blot. Results： Pseudoprotodioscin （60,30,15μg/ml） could inhibit OX-LDL-induced COX-2 expressions in a dose-dependent manner in HCASMC, and inhibit TLR2 expres- sion and p38MAPK activity. Conclusion： Pseudoprotodiosein inhibits OX-LDL-induced COX-2 expression possibly via affecting the TLR2/ MAPK pathway, which may be one mechanism for pseudoprotodioscin in inhibiting OX-LDL-induced inflammatory injury in human coronary artery vascular smooth muscle.
出处
《中药药理与临床》
CSCD
北大核心
2017年第2期31-34,共4页
Pharmacology and Clinics of Chinese Materia Medica
基金
国家科技部"十二五"重大新药创制专项资助项目"中药欧盟注册研究"(2012ZX09101231)
