摘要
目的对高糖致大鼠视网膜神经细胞凋亡的磷脂酰肌醇3-激酶-蛋白激酶(PI3K-AKT)通路机制及PKA/PKC的调控作用进行研究,为相关疾病治疗提供参考。方法细胞随机分为4组:对照组、高糖组、蛋白激酶A(PKA)抑制剂H89组和蛋白激酶C(PKC)抑制剂H7组(n=9)。除对照组外,其余各组细胞给予10 mmol·L^(-1)高糖溶液处理6 h,PKA抑制剂H89组和PKC抑制剂H7组细胞分别于最后4 h加入H89(10 mmol·L^(-1))和H7(10 mmol·L^(-1)),共培养,免疫印迹法或免疫细胞化学法分析细胞凋亡状态及PI3K-AKT和结缔组织生长因子(CTGF)的表达。结果高糖组细胞发生明显的细胞凋亡,且PI3K-AKT和CTGF的表达明显增强,而PKA抑制剂H89组上述异常显著恢复(P<0.05)。结论激活的PI3K-AKT通路及CTGF参与了高糖诱导的视网膜神经细胞凋亡过程,且其是由PKA调控的。
Objective To explore the participation of PI3K-AKT pathway in the apoptosis of retinal neural cells induced by high glucose and the modulation of PKA/PKC. Methods Retinal neural cells were divided into 4 groups randomly： a control group, a high glucose group, an H89 group, and an H7 group（n = 9）. The cells were incubated with high glucose（10 mmol·L^-1） for 6 h except the control group. Cells in the H89 and the H7 group were incubated with corresponding drugs at the last 4 h. The expressions of PI3 K, AKT, CTGF, and apoptotic related proteins were assayed. Results Apoptosis occurred in combined increased expression of PI3 K, AKT and CTGF after the medication of high glucose and PKA medication could normalize those abnormalities greatly（P〈0.05）. Conclusion Activated PI3K-AKT pathway is involved in the apoptosis of retinal neural cells induced by high glucose, which is mediated by PKA.
出处
《中南药学》
CAS
2017年第5期600-603,共4页
Central South Pharmacy
