Objective To investigate whether Irbesartan attenu ate high glucose-induced inflammation and apoptosis in H9C2 cells through inhibiting nuclear factor-kappak B(NF-kB). Methods The H9C2 cells were divided into 5 groups:control group (5.5 mmol/L glucose),mannitol group (5.5 mmol/L glucose+27.5 mmol/L mannitol),DMSO group (5.5 mmol/L glucose+1‰ DMSO),high glucose group (33 mmol/L glucose),Irbesartan group (33 mmol/L glucose +1 μmol/L Irbesartan).The inhibition rate of H9C2 cells,IL-6,MCP-1,TNF-α,Bax,Bcl-2,NF-kB,caspase-3 and the cell apoptosis were compared among these groups. Results Irbesartan significantly attenuated the high glucose-induced increase in Bax[(50.31±2.18) vs (61.96±4.08)],IL-6[(7.67±1.53) vs (25.33±4.16)],MCP-1[(26.67±6.11) vs (43.33±3.06)],TNF-α[(35.33±3.06) vs (44.67±4.16)],NF-kB[(2.19±0.52) vs (3.58±0.53)],caspase-3[(2.28±0.10) vs (2.86±0.12)]and cell apoptosis[(10.73±1.78) vs (16.46±2.24)](P<0.05),up-regulated Bcl-2 mRNA[(0.62±0.04) vs (0.45±0.06)]. Conclusion Irbesartan can attenuate high glucose-induced inflammation and apoptosis in H9C2 cells through NF-kB signaling pathway.%目的 探讨厄贝沙坦通过抑制核转录因子kB(NF-kB)的表达减轻高糖诱导的H9C2细胞炎症反应及凋亡. 方法 将H9C2细胞分为:对照(Con)组(5.5 mmol/L葡萄糖)、甘露醇(Man)组(5.5 mmol/L葡萄糖+27.5 mmol/L甘露醇)、二甲基亚砜(DMSO)组(5.5 mmol/L葡萄糖+1‰二甲基亚砜)、高糖(HG)组(33 mmol/L葡萄糖)、厄贝沙坦(Ir)组(33 mmol/L葡萄糖+1 μmol/L厄贝沙坦),每组3个细胞.检测细胞增殖抑制率;IL-6、单核细胞趋化蛋白1(MCP-1)、TNF-α、Bax、Bcl-2 mRNA;核转录因子kB(NF-kB)、caspase-3蛋白表达及细胞凋亡率. 结果 Ir组低于高糖诱导的Bax[(50.31±2.18) vs (61.96±4.08)]、IL-6[(7.67±1.53) vs (25.33±4.16)]、MCP-1[(26.67±6.11) vs (43.33±3.06)]、TNF-α[(35.33±3.06) vs (44.67±4.16)]、NF-kB[(2.19±0.52) vs (3.58±0.53)]及caspase-3[(2.28±0.10) vs (2.86±0.12)]表达及细胞凋亡[(10.73±1.78) vs (16.46±2.24)],差异均有统计学意义(P<0.05);上调高糖抑制的Bcl-2[(0.62±0.04) vs (0.45±0.06)]的表达(P<0.05). 结论 厄贝沙坦通过NF-kB信号通路,可减轻高糖诱导的H9C2细胞炎症反应及凋亡.
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