机构地区:[1]华北理工大学附属医院心血管内科,河北唐山063000
出 处:《现代生物医学进展》2024年第20期3836-3838,3866,共4页Progress in Modern Biomedicine
基 金:河北省卫健委2023年度医学科学研究课题计划项目(20231251)。
摘 要:目的:探讨纳-葡萄糖共转运蛋白2抑制剂(SGLT-2i)调控TLRs/My D88通路对高糖诱导的人主动脉内皮细胞(HAECs)自噬及凋亡的影响。方法:选用HAECs,将细胞分为NG组(5.5 mmol/L葡萄糖)、HG组(30 mmol/L葡萄糖)和SGLT-2i+HG组(30mmol/L葡萄糖+50μmol/L的SGLT-2抑制剂)。检测出各细胞生长活力、细胞凋亡水平、细胞TLRs、My D88 m RNA表达水平,细胞TLRs、My D88、Bax、Bcl-2、Beclin 1、LC3II蛋白表达以及自噬水平。结果:与NG组相比,HG组细胞增值率显著降低(P<0.05);与HG组相比,SGLT-2i+HG组细胞增值率显著上升(P<0.05)。12 h时24 h时时间点,与NG组相比,HG组细胞凋亡率均显著升高(P<0.05);与HG组相比,SGLT-2i+HG组细胞凋亡率均显著下降(P<0.05)。与NG组相比,HG组凋亡相关蛋白Bax、Bcl-2蛋白表达水平升高(P<0.05);与HG组相比,SGLT-2i+HG组细胞Bax、Bcl-2表达水平下降(P<0.05)。与NG组相比,HG组自噬相关蛋白Beclin 1、LC3II水平升高(P<0.05);与HG组相比,SGLT-2i+HG组细胞Beclin 1、LC3II水平下降(P<0.05)。与NG组相比,HG组TLRs、My D88蛋白表达水平升高(P<0.05);与HG组相比,SGLT-2i+HG组细胞TLRs、My D88表达水平下降(P<0.05)。结论:SGLT-2通过调控TLRs My D88通路抑制高糖诱导的人主动脉内皮细胞自噬及凋亡。Objective:To investigate the effect of sodium glucose cotransporter 2 inhibitor(SGLT-2i)regulating the TLRs/My D88pathway on high glucose induced autophagy and apoptosis in human aortic endothelial cells(HAECs).Methods:Using HAECs,the cells were divided into NG group(5.5 mmol/L glucose),HG group(30 mmol/L glucose),and SGLT-2i+HG group(30 mmol/L glucose+50)μMol/L of SGLT-2 inhibitor.Detect the growth vitality;the level of cell apoptosis;the expression levels of TLRs and My D88 m RNA;the levels of TLRs,My D88,Bax,Bcl-2,Beclin 1,and LC3II in each group of cells.Results:Compared with the NG group,the cell proliferation rate of the HG group was significantly reduced(P<0.05);Compared with the HG group,the SGLT-2i+HG group showed a significant increase in cell proliferation rate(P<0.05).At 12 hours and 24 hours,compared with the NG group,the apoptosis rate of cells in the HG group was significantly increased(P<0.05);Compared with the HG group,the apoptosis rate of SGLT-2i+HG group was significantly reduced(P<0.05).Compared with the NG group,the expression levels of apoptosis related proteins Bax and Bcl-2 in the HG group increased(P<0.05);Compared with the HG group,the expression levels of Bax and Bcl-2 in cells of the SGLT-2i+HG group decreased(P<0.05).Compared with the NG group,the levels of autophagy related proteins Beclin 1 and LC3II in the HG group increased(P<0.05);Compared with the HG group,the levels of Beclin 1 and LC3II in cells of the SGLT-2i+HG group decreased(P<0.05).Compared with the NG group,the expression levels of TLRs and My D88 proteins in the HG group increased(P<0.05);Compared with the HG group,the expression levels of TLRs and My D88 in the SGLT-2i+HG group decreased(P<0.05).Conclusion:SGLT-2 inhibits high glucose induced autophagy and apoptosis in human aortic endothelial cells by regulating the TLRs My D88 pathway.
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