摘要
目的探讨氯吡格雷抗动脉粥样硬化作用的潜在机制。方法经ox-LDL、氯吡格雷、PKC-θsiRNA干预后,使用液体闪烁计数检测人巨噬细胞胆固醇外流率变化,使用RT-PCR及Westbotting方法检测CD36、SR-A、PKC-θ基因表达变化。结果 ox-LDL干预后,人巨噬细胞载脂蛋白A-I和HDL-介导的胆固醇外流率下调,而巨噬细胞CD36、SR-A、PKC-θ基因的mRNA和蛋白表达水平显著增加。氯吡格雷干预后,ox-LDL诱导的人巨噬细胞CD36、SR-A、PKC-θ基因表达受到抑制。用si-RNA干扰PKC-θ表达后,提示PKC-θ参与氯吡格雷抑制ox-LDL诱导的人巨噬细胞CD36、SR-A基因的表达。结论提示氯吡格雷通过PKC-θ-依赖的途径,下调CD36、SR-A的表达,促进人巨噬细胞胆固醇外流,从而发挥抗动脉粥样硬化的作用。
Objective To explore the underlying mechanism of clopidogrel for antiatherosclerotic. Methods the ox - LDL,clo- pidogrel and PKC - θ by siRNA were down - regulated, and the macrophage cholesterol outflow rate were detected by using liquid scintil- lation,and the expression of CD36, SR - A and PKC - θ were examined by using RT - PCR and Westbotting, respectively. Results Down - regulation of ox - LDL reduced cholesterol outflow rate which regulated by A - I - and HDL, but increased the expres- sion levels of CD36, SR - A and PKC - θ. In addition, down - regulation of clopidogrel resulted CD36, SR - A, PKC - θ suppression which induced by ox - LDL. Suppressing the PKC - θ expression indicates that the PKC - θ played an important role in clopidogrel sup- pressing human macrophage CD36 and SR - A expression induced by ox - LDL. Conclusion This study indicates the mechanism of clo- pidogrel antiatherosclerotic partly, by involving PKC - θ signaling pathway, through down - regulating the CD36 and SR - A expression and promoting human macrophage cholesterol outflow.
出处
《宁夏医学杂志》
CAS
2014年第11期985-987,共3页
Ningxia Medical Journal
基金
宁夏自然科学基金资助项目(NZ13038)
