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目的研究单唾液四己糖神经节苷脂(Monosialoganglioside,GM1)对大鼠局灶性脑缺血再灌注损伤后神经功能缺失评分及Caspase-3表达的影响,探讨其神经保护作用机制。方法42只Wistar雄性大鼠随机分为三组,即神经节苷脂GM1治疗组,脑缺血再灌注损伤模型组,正常对照组。采用改良线栓法建立右侧大脑中动脉缺血再灌注模型。治疗组缺血即刻腹腔注射30mg/kg神经节苷脂,模型组注射等剂量生理盐水,运用Zea-Longa法进行神经病学评分,用光镜观察脑组织形态学改变,用免疫组化法检测Caspase-3。结果与模型组相比,GM1治疗组脑组织变性坏死程度轻,神经功能缺损评分显著减少,Caspase-3阳性细胞减少(P<0.01);模型组Caspase-3表达明显多于对照组(P<0.01),而且缺血再灌注24h较再灌注1h明显增多(P<0.01)。结论GM1可以通过抑制Caspase-3的表达来抑制细胞凋亡,从而发挥脑缺血再灌注损伤的保护作用。
Objective To investigate the effects of monosialoganglioside (GM1) on neurological deficit scores and Caspase-3 expression after focal cerebral ischemia-reperfusion injury in rats and to explore its neuroprotective mechanism. Methods Forty-two Wistar male rats were randomly divided into three groups: ganglioside GM1 treatment group, cerebral ischemia-reperfusion injury model group and normal control group. The right middle cerebral artery occlusion (MCAO) model was established by modified suture method. The rats in the treatment group were intraperitoneally injected with 30mg / kg ganglioside immediately after ischemia, the rats in the model group were injected with normal saline, the neurological score was evaluated by Zea-Longa method, the morphological changes of brain were observed with light microscope, the expressions of Caspase -3. Results Compared with the model group, the degree of degeneration and necrosis of brain tissue in GM1 treatment group was mild, the score of neurological deficit was significantly decreased and the number of Caspase-3 positive cells was decreased (P <0.01). Caspase-3 expression in model group was significantly higher than that in control group (P < 0.01), and 24h after ischemia-reperfusion was significantly increased compared with 1h after reperfusion (P <0.01). Conclusion GM1 can inhibit apoptosis by inhibiting the expression of Caspase-3, and thus protect the cerebral ischemia-reperfusion injury.