摘要
目的 观察虎杖苷对缺血缺氧作用下血管平滑肌细胞(VSMC)蛋白激酶C(PKC)活性的影响以探讨其抗休克作用的机制。方法 取大鼠胸主动脉培养VSMC,用Koyama方法复制VSMC缺血缺氧模型。用液体闪烁计数仪测定PKC的活性。结果 缺血缺氧状态下VSMC胞浆PKC的活性上升(vs正常组P<0 .05),但胞膜的PKC活性下降(vs正常组P<0 .05),经PD治疗后胞浆PKC的活性下降(vs缺血缺氧组、治疗对照组P<0. 05,vs正常组P>0 05 ),胞膜的PKC活性上升(vs缺血缺氧组、治疗对照组P<0 .05,vs正常组P>0 .05)。结论 PD对缺血缺氧作用下的VSMCPKC的活性有调节作用,这可能是PD抗休克作用的分子机制之一。
Aim To study the influence of PD on the activity of PKC(protein kinase C) of VSMC during ischemia and hypoxia.Methods The hypoxia model was made by drawing off the oxygen of an enclosed acryl glass box and ischemia model was made by low sugar culture medium. Then the activity of PKC was measured by γ-scintillation counting instrument.Results It was found that the activity of PKC of cytoplasm in VSMC in ischemia and hypoxia situation increased (vs normal group P<0.05),but the activity of PKC of cell membrane decreased(vs normal group P<0.05).When VSMC was treated with PD, the activity of PKC of cytoplasm in VSMC decreased and that of cell membrane increased (vs ischemia and hypoxia group P<0.05, vs normal group P>0.05 ).Conclusion PD can reverse the PKC activities induced by ischemia and hypoxia. It may be one of the mechanisms of PD to have antishock effect.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2005年第4期461-464,共4页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助项目(No39870936)
关键词
缺血
缺氧
平滑肌细胞
虎杖苷
蛋白激酶C
ischemia
hypoxia
vascular smooth muscle cells
protein kinase C
polydatin
