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目的 研究胰蛋白酶抑制剂在大鼠局灶性脑缺血再灌注损伤中的脑保护作用及其分子机制。方法 采用线栓法建立大鼠大脑中动脉 (MCAO)缺血 1h再灌注 2 4h模型 ,2 4只雄性大鼠随机分为假手术组、生理盐水对照组和胰蛋白酶抑制剂治疗组。采用Zea -Longa评分法观察神经功能缺损程度 ,采用免疫组织化学方法、TUNEL法分别观察各组P53 蛋白表达和细胞凋亡。结果 神经功能缺失评分假手术组为 0分 ,生理盐水对照组为 2 8± 1 0分 ,胰蛋白酶抑制剂治疗组为 1 3± 0 7分 ;P53 蛋白染色阳性细胞数假手术组为 0个 ,生理盐水对照组为 12 3± 2 5个 /高倍视野 ,胰蛋白酶抑制剂治疗组为 5 5± 1 3个 /高倍视野 ;凋亡细胞数假手术组为 0个 /高倍视野 ,生理盐水对照组为 7 6± 1 0个 /高倍视野 ,胰蛋白酶抑制剂治疗组 3 5± 0 9个 /高倍视野。胰蛋白酶抑制剂治疗组各项数据均较生理盐水对照组显著减少 ( P <0 0 1)。结论 胰蛋白酶抑制剂可明显减轻局灶性脑缺血再灌注损伤 ,抑制神经细胞P53 蛋白的表达 ,抑制细胞凋亡 ,是脑保护作用的分子机制之一。
Objective To study the neuroprotective effect of trypsin inhibitor on focal cerebral ischemia-reperfusion injury in rats and its molecular mechanism. Methods The rat model of MCAO was established by reperfusion for 24 hours. The rats were randomly divided into sham operation group, saline control group and trypsin inhibitor group. Zea-Longa score was used to observe the degree of neurological deficit. Immunohistochemistry and TUNEL method were used to observe the expression of P53 protein and apoptosis in each group. Results The neurological deficit score was 0 in sham operation group, 28 ± 10 in saline control group and 13 ± 0 7 in trypsin inhibitor group. There were 0 in P53 positive cells in sham operation group , Saline control group 12 3 ± 25 / high power field, trypsin inhibitor treatment group 5 5 ± 1 3 / high power field; the number of apoptotic cells in sham operation group 0 / high power field, saline control The group was 76 ± 1 0 high power fields and 35 ± 0 9 high power fields in the trypsin inhibitor group. The data of the treatment group with trypsin inhibitor were significantly lower than those of the saline control group (P <0.01). Conclusion Trypsin inhibitor can obviously reduce the focal cerebral ischemia-reperfusion injury, inhibit the expression of P53 protein and inhibit the apoptosis of neurons, which is one of the molecular mechanisms of brain protection.