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目的探讨锰卟啉(MnTBAP)对大鼠局灶性脑缺血损伤的保护作用及其可能机制。方法采用线拴法建立大鼠大脑中动脉栓塞(MCAO)模型,分为假手术组、缺血组、MnTBAP治疗组。缺血组和治疗组术后立即腹腔注射生理盐水和MnTBAP(10mg/kg体重),缺血24h后处死,用原位末端标记技术(TUNEL)和免疫组织化学方法对缺血侧脑组织神经细胞凋亡和凋亡调控蛋白Caspase-3表达进行检测。结果与假手术组相比,缺血组脑组织神经细胞凋亡及Caspase-3蛋白表达水平明显增加(P<0.01);与缺血组相比,MnTBAP治疗组神经细胞凋亡及Caspase-3蛋白表达水平显著减少。结论 MnTBAP能下调Caspase-3蛋白表达,抑制脑组织神经细胞凋亡,对缺血性脑损伤具有保护作用。
Objective To investigate the protective effect of manganese porphyrin (MnTBAP) on focal cerebral ischemia in rats and its possible mechanism. Methods The model of middle cerebral artery occlusion (MCAO) in rats was established by the tethering method and divided into sham operation group, ischemia group and MnTBAP treatment group. The ischemic group and the treatment group were injected intraperitoneally with normal saline and MnTBAP (10 mg / kg body weight) immediately after operation, and were sacrificed 24h after ischemia. TUNEL and immunohistochemistry were used to detect the expression of neuronal cells Apoptosis and apoptosis-regulating protein Caspase-3 expression were detected. Results Compared with the sham-operation group, the apoptosis and the expression of Caspase-3 in the brain tissue of ischemic group were significantly increased (P <0.01). Compared with the ischemia group, the apoptosis of neuron and the expression of Caspase-3 Protein expression levels were significantly reduced. Conclusions MnTBAP can down-regulate the expression of Caspase-3 protein and inhibit the apoptosis of neural cells in brain tissue, and has a protective effect on ischemic brain injury.