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目的:探讨辛伐他汀预处理对大鼠局灶性脑缺血再灌注损伤的保护作用及其机制。方法:随机将48只雄性SD大鼠分为4组:空白对照组、假手术组、缺血再灌注组和辛伐他汀预处理组。辛伐他汀预处理组在模型制备前用辛伐他汀20mg/kg连续灌胃10d,1次/d;假手术组及缺血再灌注组用相同体积的等渗盐水连续灌胃10d。以线栓法制作大鼠大脑中动脉缺血再灌注模型,于缺血2h再灌注24h后行5分制神经功能评分,并断头取脑分别测定脑梗死体积、凋亡细胞数及Bcl-2、Bax表达。结果:与空白对照组和假手术组比较,缺血再灌注组和辛伐他汀预处理组神经功能缺损较为严重,脑梗死体积增大,凋亡细胞数目增多,Bcl-2、Bax表达增加(均P<0.01)。与缺血再灌注组相比,辛伐他汀预处理组神经功能有不同程度改善,脑梗死体积明显减小,凋亡细胞数及Bax表达降低,Bcl-2表达增高,比较差异均有统计学意义(P<0.05,P<0.01)。结论:辛伐他汀预处理对大鼠脑缺血再灌注有神经保护作用,其作用机制可能与辛伐他汀上调脑组织中Bcl-2、下调Bax表达,抑制细胞凋亡有关。
Objective: To investigate the protective effect of simvastatin preconditioning on focal cerebral ischemia-reperfusion injury in rats and its mechanism. Methods: Forty eight male Sprague-Dawley rats were randomly divided into 4 groups: control group, sham operation group, ischemia-reperfusion group and simvastatin pretreatment group. Simvastatin pretreatment group with simvastatin 20mg / kg gavage 10d, 1 / d before the model preparation; sham operation group and ischemia reperfusion group with the same volume of isotonic saline continuous gavage 10d. The rat middle cerebral artery occlusion (MCAO) model was established by thread occlusion. The neurological deficit score was measured at 2h after reperfusion for 2h after reperfusion. The volume of cerebral infarction, the number of apoptotic cells and the expression of Bcl- 2, Bax expression. Results: Compared with the blank control group and the sham-operated group, the ischemic reperfusion group and simvastatin pretreatment group had more serious neurological deficits, increased cerebral infarction volume, increased apoptotic cells and increased expression of Bcl-2 and Bax All P <0.01). Compared with the ischemia-reperfusion group, the neurological function of simvastatin group was improved to some extent, the volume of cerebral infarction was significantly reduced, the number of apoptotic cells and Bax expression were decreased, the expression of Bcl-2 was increased, the differences were statistically significant Significance (P <0.05, P <0.01). CONCLUSION: Simvastatin preconditioning can protect neurons against cerebral ischemia and reperfusion in rats. Its mechanism may be related to upregulation of Bcl-2, down-regulation of Bax and inhibition of apoptosis by simvastatin.