摘要
目的探讨厄贝沙坦通过抑制核转录因子κB(NF-κB)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+1μmol/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κB(NF-κB)、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-κB[(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-κB信号通路,可减轻高糖诱导的H9C2细胞炎症反应及凋亡。
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.
出处
《中国糖尿病杂志》
CAS
CSCD
北大核心
2017年第7期630-634,共5页
Chinese Journal of Diabetes
基金
国家自然科学基金(81160117)