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目的研究不同剂型表没食子儿茶素没食子酸酯(EGCG)对高糖诱导人脐静脉内皮细胞(HUVEC)氧化应激损伤所引起凋亡的抑制作用及人核因子-κB P65(NF-κB P65)表达的影响。方法从新鲜脐带中分离培养HUVEC。用高糖诱导HUVEC表达NF-κB P65,实验组加入不同浓度的EGCG(12.5、25、50、100、200μmol/L)进行干预,PCR检测NF-κB P65 mRNA的表达,AV-PI法检测凋亡细胞。结果高糖可诱导HUVEC凋亡,NF-κB P65表达增高;EGCG可抑制NF-κB P65的表达,降低凋亡指数,具有一定的时效关系、剂量关系。结论 EGCG可在一定程度上抑制高糖诱导的氧化应激损伤所致的细胞凋亡。EGCG可能是通过抑制高糖所致的NF-κB增高,从而调控HUVEC细胞凋亡过程,发挥对HUVEC的保护作用。
Objective To investigate the effects of different dosage forms of epigallocatechin gallate (EGCG) on the apoptosis induced by high glucose-induced oxidative stress in human umbilical vein endothelial cells (HUVECs) and the effect of human nuclear factor-κB P65 ) Expression. Methods HUVECs were isolated and cultured from fresh umbilical cord. High glucose was used to induce NF-κB P65 expression in HUVECs. The experimental groups were treated with different concentrations of EGCG (12.5,25,50,100,200μmol / L), and the expression of NF-κB P65 mRNA was detected by PCR. Dead cells. Results High glucose could induce the apoptosis of HUVEC and increase the expression of NF-κB P65. EGCG could inhibit the expression of NF-κB P65 and decrease the apoptosis index, and had some time-dependent and dose-dependent relationship. Conclusion EGCG can inhibit apoptosis induced by high glucose-induced oxidative stress injury to a certain extent. EGCG may be through the inhibition of high glucose-induced increased NF-κB, thereby regulating HUVEC apoptosis process, play a protective effect on HUVEC.