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机构地区:[1]南京医科大学附属南京第一医院麻醉科,南京210006 [2]南京医科大学第一附属医院麻醉科,南京210029 [3]南京医科大学药理学系,南京210029
出 处:《中国临床医学》2005年第6期972-974,共3页Chinese Journal of Clinical Medicine
基 金:国家人事部出国留学人员资助项目(IA0001);南京医科大学创新基金项目(MO005)
摘 要:目的:观察氯化锂预处理对沙土鼠脑缺血再灌注损伤后脑皮质区Bcl-2蛋白表达的影响。方法夹闭沙土鼠双侧颈总动脉5 min制备全脑缺血性脑损伤模型。12只沙土鼠随机分为实验组和对照组。实验组手术前连续5d给予氯化锂5 mmol/kg腹腔注射; 对照组以生理盐水代替氯化锂。分别于术后第1d将动物处死,取海马齿状回互包段制成石蜡切片,进行Bcl-2蛋白的免疫组化分析。结果:实验组脑皮质Bcl-2蛋白表达阳性面积(1452.37±418.04)μm2较对照组(1289.29±610.23)μm2明显增加(P<0.05)。结论氯化锂使脑皮质区Bcl-2蛋白表达上调,是其神经元保护作用的可能机制之一。Objective: To investigate the effect of preconditioning with lithium on the expressions of Bcl-2 proteins in gerbil after global ischemia. Methods: The transient ischemia model of gerbil global was established by clamping the bilateral common carotid arteries for 5 min. 12 gerbils were randomly divided into group LiCI (n= 6) and group Saline (n= 6). Gerbils in group LiCI were injected intraperitoneally with lithium, 5mmol/kg, once a day for 5 consecutive days. Normal saline was used instead of lithium in group saline as vehicle control. All the gerbils underwent ischemia after preconditioning , then were killed 1 day after ischemia. The brains were made into paraffin sections and were used for immunohistochemistry against Bcl-2. Results: Compared with the vehicle control group [( 1289. 29 ± 610. 23)μm^2 ], the Bcl-2 expression was upregulated in the cortex in the group LiCI [ (1452. 37 ± 418.04)μm^2 ], (P〈0. 05). Conclusion: It might be one of the mechanisms underlying the neuroprotective effect of lithium that upregulates the expression of the Bcl-2 proteins.
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