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目的观察清开灵有效组分对脑缺血不同时段脑组织转化生长因子β(TGF-β)和热休克蛋白70(HSP70)含量的影响,以期从神经保护因子环节探讨清开灵有效组分抗脑缺血损伤的机制。方法成年雄性SD大鼠,随机分成假手术对照组、模型组及清开灵有效组分各组、合方组。线栓法复制大鼠持久性大脑中动脉栓塞12、24h的局灶性脑缺血模型。酶联免疫吸附法(ELISA)检测脑组织匀浆TGF-β和HSP70含量。结果脑缺血12h和24h,大鼠脑组织TGF-β和HSP70含量显著性升高,其差异具有统计学意义(P<0.05)。脑缺血12h,黄芩苷组、珍珠母组、合方组能阻抑脑组织TGF-β表达(P<0.05);脑缺血24h,胆酸组、珍珠母组能促进脑组织TGF-β表达(P<0.05)。脑缺血12h,各给药组对脑组织HSP70表达未显示有意义的生物效应(P>0.05);脑缺血24h,合方组、黄芩苷组能有效促进脑组织HSP70含量表达(P<0.05)。结论清开灵有效组分对大鼠局灶性脑缺血具有保护作用,其机制之一可能是上调TGF-β和HSP70表达,其作用具有一定的时序性。
Objective To observe the effect of effective components of Qingkailing on the content of transforming growth factor-β (TGF-β) and heat shock protein 70 (HSP70) in different stages of cerebral ischemia in order to explore the effective components of Qingkailing from the perspective of neuroprotective factors. Mechanism of anti-cerebral ischemic injury. Methods Adult male Sprague-Dawley rats were randomly divided into sham-operated control group, model group, Qingkailing effective component group and combination group. The model of focal cerebral ischemia was established by permanent embolization for 12 and 24 hours in rats with a permanent embolization method. Enzyme-linked immunosorbent assay (ELISA) was used to detect the contents of TGF-β and HSP70 in brain homogenate. Results After 12h and 24h of cerebral ischemia, the contents of TGF-β and HSP70 in rat brain increased significantly, and the difference was statistically significant (P<0.05). At 12h after cerebral ischemia, the baicalin group, the Zhumu group, and the Hefang group could inhibit the expression of TGF-β in the brain (P<0.05). After 24 hours of cerebral ischemia, the bile acid group and the Zhumu group could promote the brain TGF-β. Expression (P<0.05). At 12h after cerebral ischemia, there was no significant biological effect on the expression of HSP70 in brain tissue in each drug group (P>0.05). In the 24h after cerebral ischemia, HSP70 content in brain tissue could be effectively promoted in combination group and baicalin group (P< 0.05). Conclusion The effective components of Qingkailing have a protective effect on focal cerebral ischemia in rats. One of the mechanisms may be to upregulate the expression of TGF-β and HSP70, which has a certain time sequence.