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目的探讨阿托伐他汀(AT)对链脲佐菌素(STZ)诱导的高血糖状态下,大脑中动脉栓塞(MCAO)性脑梗死大鼠模型中脑血管新生情况。方法选取雄性SD(sprague-dawley)大鼠36只,运用随机数字表法将之分为3组(每组大鼠数目均为12只)。分别为:正常对照组(简称NC组)、高血糖模型组(即糖尿病组,简称DM组)以及阿托伐他汀治疗组(简称DM+AT组)。本实验共2个动物模型,首先将DM组和DM+AT组SD大鼠运用STZ诱导制作高血糖模型(DM模型)。然后将这3组大鼠均用线栓法制作大脑中动脉栓塞性脑梗死模型(MCAO模型)。造模成功后,DM+AT组SD大鼠每日分别给予阿托伐他汀10 mg/(kg·d),连续灌胃14 d,DM组只给予生理盐水灌胃。期间3组SD大鼠自由饮水、摄食,不予降糖药物治疗。实验结束即第15天处死所有大鼠,免疫组化SP法测定大鼠脑组织血管内皮生长因子(VEGF)、Ⅷ因子的蛋白表达水平以及微血管密度(MVD)。结果NC、DM、DM+AT组大鼠的脑组织梗死百分比分别为(15.7±2.8)%、(23.2±2.1)%、(19.3±2.5)%;3组大鼠MVD(8.1±0.52 vs.6.4±0.38 vs.2.4±0.18)、VEGF(22.1±3.3 vs.18.7±2.3 vs.13.8±2.7)以及Ⅷ因子表达水平(10.2±2.8 vs.8.3±1.7 vs.6.3±1.3),差异均具有统计学意义。结论高血糖可抑制大鼠脑梗死后血管新生,而阿托伐他汀干预后可改善血管新生状况,这一过程可能涉及到VEGF和Ⅷ因子蛋白的表达变化。
Objective To investigate the effect of atorvastatin (AT) on angiogenesis in STZ-induced hyperglycemia in rats with middle cerebral artery occlusion (MCAO) cerebral infarction. Methods Thirty - six male Sprague - Dawley rats were randomly divided into three groups (12 rats in each group). They were: normal control group (NC group), hyperglycemia model group (DM group) and atorvastatin treatment group (DM + AT group). In this study, a total of two animal models, first DM group and DM + AT group SD rats using STZ induced hyperglycemia model (DM model). Then all the rats in the three groups were given MCAO model by middle cerebral artery occlusion (MCAO). After successful modeling, SD rats in DM + AT group were given atorvastatin 10 mg / (kg · d) daily for 14 days. Rats in DM group were given normal saline only. During the 3 groups of SD rats free access to water, food intake, not hypoglycemic drugs. At the end of the experiment, all rats were killed on the 15th day. The protein expression of vascular endothelial growth factor (VEGF) and factor Ⅷ and brain microvessel density (MVD) in rat brain were detected by immunohistochemical SP method. Results The percentage of cerebral infarction in NC, DM and DM + AT groups was (15.7 ± 2.8)%, (23.2 ± 2.1)% and (19.3 ± 2.5)%, respectively 6.4 ± 0.38 vs.2.4 ± 0.18), VEGF (22.1 ± 3.3 vs.18.7 ± 2.3 vs.13.8 ± 2.7), and the expression of factor Ⅷ (10.2 ± 2.8 vs.8.3 ± 1.7 vs.6.3 ± 1.3) Statistical significance. Conclusion Hyperglycemia can inhibit angiogenesis after cerebral infarction in rats, and atorvastatin can improve the angiogenesis after intervention, which may involve the changes of VEGF and Ⅷ factor protein expression.