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目的研究骨形态发生蛋白-7(BMP-7)对大鼠局灶性脑缺血再灌注损伤后NF-κB P65蛋白和Bax蛋白表达活性的影响。方法成年雄性Wistar大鼠50只,随机分为假手术组15只、对照组15只、BMP-7治疗组15只(去除5只造模失败的大鼠),应用线栓法制备局灶性脑缺血2h模型。再灌注同时,治疗组经尾静脉注射BMP-7(0.1mg/kg),对照组和假手术组注射等量无菌生理盐水。再灌注24h后分别对3组大鼠进行神经功能评分,三苯基氯化四氮唑(TTC)染色观察脑梗死体积,免疫组化法观察NF-κB P65和Bax蛋白表达。结果假手术组无神经功能缺损,无脑梗死发生。与对照组比较,治疗组神经功能评分明显降低,脑梗死体积百分比显著降低,差异有统计学意义(t=5.18、13.43,P<0.05);缺血侧海马内NF-κB P65表达区平均光密度值明显增加,Bax蛋白表达区平均光密度值明显减少,差异有统计学意义(F=74.51、199.65,q=6.65、12.38,P<0.01)。结论 BMP-7能改善神经功能缺损,减轻脑缺血再灌注损伤,此过程可能与抑制细胞凋亡有关。
Objective To investigate the effect of bone morphogenetic protein-7 (BMP-7) on the expression of NF-κB P65 protein and Bax protein after focal cerebral ischemia-reperfusion injury in rats. Methods Fifty adult male Wistar rats were randomly divided into sham operation group (n = 15), control group (n = 15) and BMP-7 treatment group (n = 5) Cerebral ischemia 2h model. At the same time of reperfusion, BMP-7 (0.1mg / kg) was injected into the tail vein of the treatment group, and the same volume of sterile saline was injected into the control group and the sham operation group. After 24 hours of reperfusion, the neurological function score, the volume of cerebral infarction were observed by TTC staining and the expressions of P65 and Bax protein were detected by immunohistochemistry. Results Sham-operated group had no neurological deficits and no cerebral infarction. Compared with the control group, the score of neurological function in the treatment group was significantly lower, and the volume percentage of cerebral infarction was significantly lower (t = 5.18, 13.43, P <0.05). The average light intensity of NF-κB P65 expression in the hippocampus The mean optical density of Bax protein expression zone decreased significantly (P = 74.51, 199.65, q = 6.65, 12.38, P <0.01). Conclusion BMP-7 can improve neurological deficits and alleviate cerebral ischemia-reperfusion injury, which may be related to the inhibition of apoptosis.