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目的:研究黄连苷Ⅱ对大鼠脑缺血后细胞凋亡和NFκB表达的影响。方法:应用线栓法建立大鼠大脑中动脉闭塞再灌注模型,经尾静脉注射胡黄连苷Ⅱ(10mg.kg-1)干预治疗,免疫组化检测脑缺血再灌注后核转录因子κB(NFκB)表达,原位缺口末端标记(TUNEL)检测神经细胞凋亡。结果:假手术组大鼠皮质、纹状体和海马区脑组织NFκB,TUNEL阳性细胞数量较少,散在分布。模型组大鼠各区脑组织NFκB表达显著增强,吸光度值(A)和TUNEL阳性细胞数量较假手术组均显著增多(P<0.05)。胡黄连苷组各区脑组织NFκB(A值)及TUNEL阳性细胞数量均显著低于模型对照组(P<0.05)。结论:胡黄连苷Ⅱ可能通过下调NFκB的表达,抑制脑缺血再灌注损伤炎症反应导致的神经细胞凋亡。
Objective: To study the effects of marinoside Ⅱ on apoptosis and expression of NFκB after cerebral ischemia in rats. Methods: The model of middle cerebral artery occlusion and reperfusion was established by thread occlusion. The rats were injected with picrotoxin Ⅱ (10mg.kg-1) through the tail vein for the interventional therapy. The expression of nuclear factor kappa B NFκB) expression, in situ nick end labeling (TUNEL) detection of neuronal apoptosis. Results: The number of NFκB and TUNEL positive cells in the cortex, striatum and hippocampus in the sham operation group were less and scattered. The expression of NFκB in brain tissue of model group was significantly increased, the number of absorbance (A) and TUNEL positive cells were significantly increased (P <0.05) compared with those in sham operation group. The contents of NFκB (A value) and TUNEL positive cells in each group of picroside group were significantly lower than those in model control group (P <0.05). Conclusion: Picroside Ⅱ may inhibit the apoptosis of neural cells induced by inflammatory reaction after cerebral ischemia-reperfusion injury by down-regulating the expression of NFκB.