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目的:探索蝎毒耐热蛋白(SVHRP)对淀粉样β蛋白(Aβ)神经毒性的抑制作用。方法:在大鼠海马内每侧注射Aβ1-40(10μg/2μl)后1d,给予腹腔SVHRP(0.5～2μg/100g),1次/d,连续10次。建模16d后分别进行海马部位的突触体素免疫组织化学分析和突触超微结构计量观察。结果:与对照组比较,Aβ组大鼠突触体素免疫反应强度和电镜下突触密度明显下降(P<0.01),小突触丢失为主,突触终末可见突触小泡大量集聚,突触活性区平均长度增加。SVHRP干预组大鼠实触体素免疫反应强度和电镜下突触密度明显高于Aβ组大鼠(P<0.01),突触终末内未见突触小泡过量集聚,但小突触比例显著增加(P<0.01)。结论:以上结果强有力的提示,Aβ是突触退变的始动因素,SVHRP可抑制Aβ引起的突触退变,有可能成为治疗Alzheimer病(AD)的一种药物。
Objective: To explore the inhibitory effect of SVHRP on neurotoxicity of amyloid β protein (Aβ). Methods: Intraperitoneal injection of SVHRP (0.5 ~ 2μg / 100g) was given to rats intraperitoneally once a day for 1 d after injection of Aβ1-40 (10μg / 2μl) into the hippocampus of rats. Sixteen days after modeling, synaptophysin immunohistochemistry and synaptic ultrastructure were observed in the hippocampus. Results: Compared with the control group, the intensity of synaptophysin immunoreactivity and the density of synapse in the Aβ group were significantly decreased (P <0.01), and the loss of synapse was dominant. The synaptic vesicles , The average length of synaptic active area increased. Compared with Aβ group (P <0.01), the intensity of real-touch voxel immunosuppression in SVHRP-treated group was significantly higher than that in Aβ group (P <0.01), and no synaptic vesicles accumulated in synaptic terminals, but the synaptic proportion Significantly increased (P <0.01). Conclusion: The above results strongly suggest that Aβ is the initiating factor of synaptic degeneration. SVHRP can inhibit the synaptic degeneration induced by Aβ and may become a drug for the treatment of Alzheimer’s disease (AD).