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目的探讨新型降血脂药rosuvastatin对缺血性脑损伤的保护作用及机制。方法用腔内线栓法制造小鼠脑缺血再灌注动物模型,用脑血流激光多普勒监测脑缺血过程中脑血流的变化,用甲酚紫染色法显示脑梗死区并用imageJ软件计算梗死体积和脑水肿,用Western blot分析脑缺血前后内皮型一氧化氮合酶(eNOS)和活化的caspase-3(activated caspase-3)的变化,用免疫组织化学方法观察rosuvastatin对脑缺血再灌注后诱导型一氧化氮合酶(iNOS)的影响。结果Rosuvastatin 20mg/kg可以明显减少梗死体积,减轻脑水肿。脑缺血前脑组织eNOS表达为(100±43.3)%,缺血后明显升高至(1668.9±112.2)%(P<0.001),使用rosuvastatin后非缺血区脑组织eNOS表达为(511.4±68.7)%,缺血区脑组织eNOS表达为(1678.8±121.3)%。非缺血区皮层无活化的caspase-3表达,脑缺血后活化的caspase-3表达上升,rosuvastatin可使之显著降低(P<0.01)。免疫组织化学染色显示非缺血脑组织无iNOS阳性细胞表达,脑缺血再灌注后iNOS表达增多,rosuvastatin可明显减少iNOS的表达。结论Rosuvastatin可能通过增加eNOS、抑制iNOS和活化的caspase-3的表达而起到神经保护作用。
Objective To investigate the protective effect of rosuvastatin on ischemic brain injury and its mechanism. Methods The model of cerebral ischemia-reperfusion in mice was made by the method of intraluminal thread occlusion. The changes of cerebral blood flow during cerebral ischemia were monitored by cerebral blood flow laser Doppler. Cerebral infarction area was observed by cresyl violet staining and imageJ software was used The infarction volume and brain edema were calculated. The changes of eNOS and activated caspase-3 before and after cerebral ischemia were detected by Western blot. The effects of rosuvastatin on brain ischemia Effect of inducible nitric oxide synthase (iNOS) after blood reperfusion. Results Rosuvastatin 20mg / kg can significantly reduce infarct volume, reduce cerebral edema. The expression of eNOS in cerebral ischemia preconditioning group was (100 ± 43.3)%, significantly increased to (1668.9 ± 112.2)% after ischemia (P <0.001). The eNOS expression in nonischemic brain tissue after rosuvastatin administration was (511.4 ± 68.7%), eNOS expression in ischemic brain tissue was (1678.8 ± 121.3)%. The expression of caspase-3, which was not activated in non-ischemic cortex, increased after activation of caspase-3, and rosuvastatin significantly decreased (P <0.01). Immunohistochemical staining showed that no iNOS positive cells were expressed in non-ischemic brain tissue. The expression of iNOS increased after cerebral ischemia and reperfusion, and rosuvastatin significantly reduced iNOS expression. Conclusion Rosuvastatin may play a neuroprotective role by increasing eNOS, inhibiting the expression of iNOS and activating caspase-3.