摘要
目的观察尤瑞克林对缺血性脑卒中大鼠bcl-2、bax蛋白表达的影响,探讨尤瑞克林抑制神经细胞凋亡保护缺血性脑损伤的可能作用机制,为尤瑞克林治疗缺血性脑卒中在临床上的应用提供更深层次的理论依据。方法选用健康SD大鼠,随机分为假手术组、单纯缺血组、尤瑞克林低、中、高3个剂量组,每组12只。制作大鼠局灶性脑缺血模型,术后30min及23.5h尤瑞克林低、中、高剂量组舌下静脉注射尤瑞克林3.75×10-3、8.75×25-3、17.25×10-3PNA单位/kg,余2组以同样给药途径予等剂量0.9%氯化钠溶液。24h后行神经功能缺损评分;免疫组化法行凋亡相关基因bcl-2、bax蛋白定量分析。结果单纯缺血组动物神经功能缺损评分最为严重,尤瑞克林不同剂量组神经功能缺损评分均明显低于单纯缺血组(P<0.05或<0.01)。尤瑞克林各组与单纯缺血组比较,bcl-2蛋白表达升高(P<0.05或<0.01)、同时bax蛋白表达降低(P<0.05或<0.01),且随剂量升高呈量效关系。结论尤瑞克林对缺血性脑损伤具有保护作用,其作用机制可能与提高bcl-2蛋白表达、抑制bax蛋白表达而减轻细胞凋亡来减少脑缺血后迟发性神经元损伤。
Objective To observe the effect of urokallikrein on the expression of bcl-2 and bax protein in rats with focal cerebral ischemia,and to explore the potential action mechanism of urokallikrein in inhibiting nerve cell apoptosis and protecting ischemic cerebral injury so as to provide theoretical basis for the clinical application of urokallikrein in treating cerebral ischemic stroke. Methods The 60 healthy SD rats were randomly divided into 5 groups ： sham operation group, simple ischemia group, high-dose, median-dose, low-dose urokallikrein group, with 12 rats in each group. After the rat models with focal cerebral ischemia were established, the rats in high-dose, median-dose,low-dose urokallikrein group were given urokallikrein by sublingual vein injection at the dosage of 3.75 ×10 -3,8.75×10 -3,17.25 ×10 -3 PNA Unit/kg on 30 minutes and 23.5 hours after operation, respectively, however,the rats in the other two groups were given 0.9% sodium chloride solution of same volume by sublingual vein injection. The neurologic impairment scoring was performed 24h after operation, and quantitative analysis of bcl-2 and bax protein was carried out by immunohistochemistry, and the damages of nerve cells were evaluated by HE staining. Results The neurologic impairment scoring in simple ischemia group was highest among 5 groups, however,which in three different dose urokallikrein groups was significantly lower than that in simple ischemia group （ P 〈0.05 or P 〈0.01 ）. As compared with those in simple ischemia group,the expression levels of bcl-2 protein in three different dose urokallikrein groups were significantly increased （ P 〈 0.05 or P 〈 0.01 ）, but the expression levels of bax protein in three different dose urokallikrein groups were significantly decreased （ P 〈 0.05 or P 〈0.01 ）, furthermore, which had a dose -effect relationship. Conclusion The urokallikrein has protective effect on focal ischemic cerebral injury, and its action mechanism may be related with increasing the expression of
出处
《河北医药》
CAS
2013年第13期1934-1936,共3页
Hebei Medical Journal
关键词
脑缺血
细胞凋亡
尤瑞克林
大鼠
cerebral ischemia
cell apoptosis
urokallikrein
rats
