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目的研究ATP敏感的钾离子通道开放剂二氮嗪(diazoxide)预处理对Aβ1~42作用原代培养神经元N-甲基-D-天冬氨酸(NMDA)受体2B(NR2B)亚基蛋白表达的影响。方法原代培养大鼠皮层海马神经元并进行鉴定,将细胞随机分为对照组、单纯Aβ1~42干预组、二氮嗪预处理1h后Aβ1~42干预组(Aβ1~42+diazoxide)、单纯二氮嗪预处理组,并采用免疫印迹检测不同时间点(24 h、72 h)细胞NR2B亚基蛋白表达水平的变化。结果 Aβ1~42(2μmol/L)作用神经元24 h后,与对照组相比,单纯Aβ1~42干预组和Aβ1~42+diazoxide组的NR2B亚基蛋白表达均无明显改变。Aβ1~42作用神经元72 h后,与对照组比较,单纯Aβ1~42组NR2B亚基蛋白表达量显著升高(P<0.05);而与单纯Aβ1~42干预组相比,Aβ1~42+diazoxide组NR2B亚基蛋白表达明显降低(P<0.05)。结论 Aβ1~42作用原代培养神经元72 h,能够显著增加神经细胞NR2B亚基蛋白的表达量;同时,二氮嗪能拮抗Aβ1~42所引起的NR2B亚基蛋白表达量升高,提示二氮嗪可能通过NMDA受体通路影响Aβ1~42的细胞毒性作用。
Objective To investigate the effects of ATP-sensitive potassium channel opener diazoxide pretreatment on the expression of N-methyl-D-aspartate (NMDA) receptor 2B (NR2B) subunit Effect of protein expression. Methods Primary cultured rat cortical hippocampal neurons were identified and identified. The cells were randomly divided into control group, Aβ1 ~ 42 intervention group, Aβ1 ~ 42 intervention group (Aβ1 ~ 42 + diazoxide) Diazoxide preconditioning group. Western blotting was used to detect the expression of NR2B subunit protein at different time points (24 h and 72 h). Results Compared with the control group, the expression of NR2B subunit protein in Aβ1 ~ 42 intervention group and Aβ1 ~ 42 + diazoxide group was not changed after Aβ1 ~ 42 (2μmol / L) treatment for 24 h. Compared with the control group, the expression of NR2B subunit protein in Aβ1 ~ 42 group was significantly increased (P <0.05) at 72 h after Aβ1-42 treatment, but compared with Aβ1 ~ 42 intervention group, Aβ1 ~ 42 + Diazoxide group NR2B subunit protein expression was significantly reduced (P lt; 0.05). Conclusion Aβ1-42 can significantly increase the expression of NR2B subunit protein in primary cultured neurons for 72 h. At the same time, diazoxide can antagonize the increase of NR2B subunit protein expression induced by Aβ1-42, Azadiazine may affect the cytotoxic effect of Aβ1-42 through the NMDA receptor pathway.