NF-κB在高糖诱导“代谢记忆”致心肌细胞损伤的作用机制

NF-κB in High Glucose-induced "metabolic memory" Induced Myocardial Cell Injury Mechanisms

目的探讨代谢记忆损伤心肌细胞的分子机制。方法体外培养20只SD大鼠乳鼠心肌细胞,每组5只,分为4组:持续低糖组、持续高糖组、代谢记忆组和PDTC组。计算细胞凋亡指数,免疫组化检测核内NF-κB的表达,Western Blot检测NF-κB蛋白,TUNEL检测细胞凋亡。结果代谢记忆组蛋白表达水平(15.12±2.32)和持续高糖组的(17.10±3.12)均较持续低糖组(5.23±2.13)的NF-κB核内蛋白水平显著升高(P<0.01),PDTC预处理后,NF-κB核内蛋白水平(7.12±2.41)较代谢记忆组(17.10±3.12)显著降低(P<0.05);同时,代谢记忆组(19.42±3.22)和持续高糖组(22.36±3.45)凋亡指数较持续低糖组(8.56±0.23)有明显的增加(P<0.05),而PDTC组(10.33±1.34)较代谢记忆组心肌细胞凋亡指数(19.42±3.22)有明显降低(P<0.05)。结论 PDTC能抑制代谢记忆中所致的心肌细胞的损伤,NF-κB的激活可能介导了高糖诱导的代谢记忆所致的心肌细胞的损伤。

Objective Discussion on metabolic memory of the molecular mechanisms of myocardial cell injury.Methods 20 SD rats were cultured neonatal rat cardiomyocytes,n=5,divided into four groups：continuous low-sugar group;sustained high glucose group;metabolic memory group;PDTC group.Calculated apoptotic index,immunohistochemical nuclear expression of NF-κB,Western Blot test NF-κB protein,TUNEL detection of apoptosis.Results Metabolic memory（15.12±2.32）and sustained high group（17.10±3.12）levels of protein expression of the glucose group compared with continuous low-sugar group（5.23±2.13） of NF-κB nuclear protein levels were significantly increased（P0.01）,PDTC（7.12±2.41） pretreatment,NF-κB nuclear protein levels compared with significantly lower metabolic memory（17.10±3.12）;the same time,metabolic memory group（19.42±3.22） and the apoptotic index of sustained high glucose group（22.36±3.45） compared with continuous low-sugar group（8.56±0.23） significantly increased（P0.05）,while PDTC group（10.33±1.34） than in metabolic memory myocardial（19.42±3.22） apoptosis index decreased significantly（P0.05）.Conclusion PDTC can inhibit the metabolism of the memory of the damage caused by myocardial cells,NF-κB activation might be mediated by high glucose-induced metabolic memory induced myocardial cell injury.