摘要
目的观察电针对糖尿病模型大鼠海马CA3区核因子E2相关因子(Nrf2)、血红素氧合酶(HO-1)与突触后致密蛋白95(PSD95)表达变化,探讨电针保护糖尿病神经系统损伤的可能机制。方法将雄性Wistar大鼠随机分为正常组、载体组、糖尿病组和电针组,每组8只。采用链脲佐菌素腹腔注射法制备糖尿病大鼠模型。造模成功1周后,电针组电针刺激一侧“足三里”及“胰俞”穴,30分钟/次,1次/天,连续4周。血糖仪检测大鼠空腹血糖水平;尼氏染色法观察大鼠海马CA3区神经元形态;免疫组织化学染色法检测大鼠海马CA3区的Nrf2、HO-1与PSD95的蛋白表达。结果空腹血糖检测结果显示,与正常组和载体组比较,糖尿病组血糖水平升高(P<0.05);与糖尿病组比较,电针组血糖水平降低(P<0.05)。尼氏染色结果显示,与正常组和载体组比较,糖尿病组海马CA3区神经元层次减少,胞核固缩;与糖尿病组比较,电针组海马CA3区神经元层次增加,形态改善。免疫组织化学染色结果显示,与正常组和载体组比较,糖尿病组海马CA3区Nrf2、HO-1与PSD95蛋白表达降低(P<0.05);与糖尿病组比较,电针组海马CA3区Nrf2、HO-1与PSD95蛋白表达升高(P<0.05),且与正常组和载体组表达水平相接近(P>0.05)。结论电针可上调糖尿病模型大鼠海马CA3区Nrf2、HO-1与PSD95的表达,提示其可能通过抑制氧化应激和改善突触可塑性发挥对其对神经元的保护作用。
Objective To observe the effect of electroacupuncture(EA)on the expression changes of nuclear factor E2 related factors(Nrf2),heme oxygenase-1(HO-1)and postsynaptic density protein 95(PSD95)in the hippocampal CA3 region of diabetic model rats,aiming to explore the possible mechanism of EA in protecting the injury of diabetic nervous system.Methods Male Wistar rats were randomly divided into a normal group,a vector group,a diabetic group and an EA group,with 8 rats in each group.The diabetic model was established by intraperitoneal injection of streptozotocin.One week later,the EA group received EA stimulation at the acupoints of“Zusanli”and“Yishu”for 30 min,once a day for 4 weeks.The fasting blood glucose level was measured by a glucose meter.The morphology of neurons in the hippocampal CA3 region was observed by Nissl staining.The protein expressions of Nrf2,HO-1 and PSD95 in the hippocampal CA3 region were detected by immunohistochemical staining.Results Compared with the normal group and the vector group,the diabetic group had increased blood glucose level(P<0.05).Compared with the diabetic group,the EA group had decreased blood glucose level(P<0.05).Compared with the normal group and the vector group,the diabetic group had reduced layers of neurons in the hippocampal CA3 region,with pyknosis in the nuclei Compared with the diabetic group,the EA group had increased layers of neurons in the hippocampal CA3 region,with improved morphology of neurons.Compared with the normal group and the vector group,the diabetic group had decreased expressions of Nrf2,HO-1 and PSD95 in the hippocampal CA3 region(P<0.05).Compared with the diabetic group,the EA group had increased expressions of Nrf2,HO-1 and PSD95 in the hippocampal CA3 region(P<0.05),and the expression levels were similar to those of the normal group and the vector group(P>0.05).Conclusion EA can up-regulate the expressions of Nrf2,HO-1 and PSD95 in the hippocampal CA3 region of diabetic model rats,suggesting that it may play a protective role on neurons by inhibiting oxidative stress and improving synaptic plasticity.
作者
王薇
龚鑫
吴锋
赵健
Wang Wei;Gong Xin;Wu Feng;Zhao Jian(Department of Anatomy,Wannan Medical College,Wuhu 241002,Anhui,China)
出处
《右江民族医学院学报》
2024年第1期37-42,共6页
Journal of Youjiang Medical University for Nationalities
基金
皖南医学院中青年科研基金(WK202125)
安徽省质量工程项目(2020SJSFJXZZ390)。
关键词
糖尿病
电针
核因子E2相关因子
血红素氧合酶
突触后致密蛋白95
海马CA3区
diabetes mellitus
electroacupuncture
nuclear factor E2 related factors
heme oxygenase-1
postsynaptic density protein 95
hippocampal CA3
