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目的:通过观察糖尿病大鼠脑缺血后,脑组织内Rac1表达的变化及其对VEGF、SDF-1表达的影响,探讨不同血糖水平时Rac1对脑缺血后血管新生的影响机制。方法:腹腔注射链脲霉素制作糖尿病大鼠脑缺血模型,尾静脉注射Rac1抑制剂NSC23766,通过western blotting法检测脑组织中总Rac1、VEGF和SDF-1表达;通过GST-pulldown法检测脑组织中活性Rac1表达。结果:在糖尿病大鼠脑缺血模型中,VEGF和SDF-1的表达随着血糖水平的升高而下降;脑组织内Rac1蛋白表达随着血糖水平升高而减少;抑制Rac1活性后,脑组织中VEGF表达均下降但SDF-1的表达反而增加。结论:在糖尿病大鼠脑缺血模型中,高血糖可抑制脑组织Rac1、VEGF和SDF-1的水平,该抑制作用随着血糖升高而增加。抑制Rac1水平可抑制VEGF表达但并未抑制SDF-1水平,提示高血糖可能通过抑制Rac1导致VEGF表达下降,从而影响血管新生。
OBJECTIVE: To investigate the effect of Rac1 on angiogenesis induced by cerebral ischemia in diabetic rats by observing the changes of Rac1 expression and the expression of VEGF and SDF-1 after cerebral ischemia in diabetic rats. Methods: The rat model of cerebral ischemia induced by streptozotocin was established by intraperitoneal injection of streptozotocin. The Rac1 inhibitor NSC23766 was injected into tail vein. The expression of Rac1, VEGF and SDF-1 in brain tissue were detected by western blotting. Active Rac1 expression in tissues. Results: The expression of VEGF and SDF-1 decreased with the increase of blood glucose level in diabetic rat model of cerebral ischemia. The expression of Rac1 protein in brain tissue decreased with the increase of blood glucose level. After inhibiting Rac1 activity, VEGF expression in the tissue decreased but the expression of SDF-1 increased. CONCLUSION: Hyperglycemia can inhibit the levels of Rac1, VEGF and SDF-1 in cerebral ischemia model of diabetic rats. The inhibition increases with the increase of blood glucose. Inhibition of Rac1 levels can inhibit the expression of VEGF but did not inhibit the SDF-1 levels, suggesting that high blood sugar may be caused by inhibition of Rac1 VEGF expression decreased, thus affecting angiogenesis.