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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 attenuates high glucose-induced inflammation and apoptosis in H9C2 cells by inhibiting the expression of nuclear factor κB (NF-κB). Methods H9C2 cells were divided into control group (5.5 mmol / L glucose), Man group (5.5 mmol / L glucose + 27.5 mmol / L mannitol), dimethyl sulfoxide group (5.5 mmol / L glucose + 1 ‰ dimethyl sulfoxide), high glucose (33 mmol / L glucose), irbesartan (33 mmol / L glucose + 1 μmol / Sartan), 3 cells per group. The expression of IL-6, MCP-1, TNF-α, Bax and Bcl-2 mRNA and the expressions of NF-κB and caspase-3 were detected by flow cytometry Rate of apoptosis. Results Compared with 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) (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) and caspase-3 ) (2.86 ± 0.12) and cell apoptosis [(10.73 ± 1.78) vs (16.46 ± 2.24)], the difference was statistically significant (P <0.05) ± 0.04) vs (0.45 ± 0.06)] (P <0.05). Conclusion Irbesartan can reduce the inflammation and apoptosis of H9C2 cells induced by high glucose through NF-κB signaling pathway.