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目的 :探讨益气通络丹治疗缺血缺氧性心血管疾病的机理。方法 :用自制的密闭有机玻璃盒抽去氧气造成大鼠VSMC(vascularsmoothmusclecell,血管平滑肌细胞 )缺氧环境 ,同时用低糖培养基造成缺血的环境 ,从而制成VSMC的缺血缺氧模型。然后用γ -闪烁计数仪测定PKC(ProteinkinaseC ,蛋白激酶C)的活性。结果 :缺血缺氧状态下平滑肌细胞胞浆PKC的活性上升 (vs正常组P <0 .0 5 ) ,但胞膜的PKC活性下降 (vs正常组P <0 .0 5 ) ,经益气通络丹治疗后胞浆PKC的活性有所下降 ,而胞膜PKC的活性有所升 ,都接近到正常的水平 (vs正常组P >0 .0 5 )。结论 :益气通络丹对缺血缺氧性心脑血管疾病的治疗作用可能与调节VSMC的PKC活性有关。
Objective : To explore the mechanism of Yiqi Tongluodan in the treatment of ischemic and hypoxic cardiovascular diseases. METHODS : Oxygen was deprivation of Oxygen to cause the hypoxic environment of rat VSMC (vascular smooth muscle cells), and the environment of ischemic injury was induced by low-glucose medium. The hypoxic-ischemic model of VSMC was established. The PKC (protein kinase C, protein kinase C) activity was then measured using a gamma-scintillation counter. RESULTS: The activity of PKC in the cytoplasm of smooth muscle cells increased during ischemic and hypoxic conditions (vs P<0.05 in normal group), but the PKC activity in the membrane decreased (vs P<0.05 in normal group). After treatment with Tongluodan, the activity of PKC in cytoplasm decreased, while the activity of membrane PKC increased. Both were close to normal levels (vs P>0.05 in normal group). Conclusion: The therapeutic effect of Yiqi Tongluo Dan on hypoxic-ischemic cardiovascular and cerebrovascular diseases may be related to the regulation of PKC activity in VSMC.