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在初级糖尿病脑病中海马神经元细胞的凋亡与认知能力相关.在本研究中,研究桃叶珊瑚苷在初级糖尿病脑病大鼠中的神经保护机制.实验大鼠被随机分为3组:空白对照组、STZ诱导糖尿病组及STZ诱导糖尿病桃叶珊瑚苷治疗组.除空白对照组以外,所有大鼠接受60mg/kg链脲佐菌素腹腔注射诱导糖尿病.桃叶珊瑚苷治疗组的大鼠在第65天开始连续腹腔注射5mg/kg的桃叶珊瑚苷,共注射15天,利用Y迷宫检测动物行为学变化.在第87天进行脑组织的组织学检测,用光学显微镜进行海马CA1区存活神经元细胞计数,应用透射电子显微镜对CA1区神经元细胞的超微结构观察和凋亡细胞数量计数.为了弄清桃叶珊瑚苷的神经保护机制,应用WesternBlot和免疫组化方法对Bcl-2和Bax两种凋亡蛋白的表达进行了分析.结果显示,桃叶珊瑚苷抑制了海马CA1区神经元细胞凋亡,并起到降低血糖浓度、增加体重、改善糖尿病大鼠的学习状况,最终使Bcl-2和Bax两种凋亡蛋白的表达比例得到了平衡.结果暗示桃叶珊瑚苷抑制神经元细胞的凋亡可能是通过调控Bcl-2和Bax两种凋亡蛋白的表达来完成.
The apoptosis of hippocampal neurons in primary diabetic encephalopathy is associated with cognitive ability. In this study, the neuroprotective mechanism of aucubin in primary diabetic encephalopathy rats was studied. Experimental rats were randomly divided into 3 groups: Control group, STZ-induced diabetes group and STZ-induced diabetes aucubin group. Except for the blank control group, all rats received 60 mg/kg streptozotocin intraperitoneally to induce diabetes. The oleoreside treatment group was large. On the 65th day, the mice were injected with 5 mg/kg aucubin continuously for 15 days. The behavioral changes of the animals were detected by the Y-maze. Histological examination of the brain tissue was performed on the 87th day and the hippocampus CA1 was examined with an optical microscope. The number of surviving neuron cells was counted, and the ultrastructure of CA1 neurons was observed by transmission electron microscopy and the number of apoptotic cells was counted. In order to clarify the neuroprotective mechanism of aucubin, Western Blot and immunohistochemistry methods were used to analyze Bcl. The expression of two apoptotic proteins, -2 and Bax, was analyzed. The results showed that euphorbia inhibited neuronal apoptosis in the hippocampal CA1 region and reduced blood glucose levels and increased body weight. The learning status of a good diabetic rat eventually balanced the expression of two apoptotic proteins, Bcl-2 and Bax. The results suggest that aucubin inhibits neuronal cell apoptosis may be through regulation of Bcl-2 and Bax. The expression of several apoptotic proteins completes.