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目的探讨丁酸钠预处理对内毒素性肝损伤小鼠细胞凋亡的影响。方法取健康雄性昆明小鼠48只,随机分为4组(各12只):正常组、模型组、联苯双酯组、丁酸钠组。应用脂多糖10 mg/kg腹腔注射小鼠诱导内毒素肝损伤模型。造模后6 h,检测小鼠血清ALT和AST活性,MDA含量和SOD活性,TUNEL法检测小鼠肝脏组织细胞凋亡情况。结果与模型组相比,丁酸钠组和联苯双酯组血清ALT、AST和MDA含量明显降低(P<0.05),SOD活性升高(P<0.05),肝细胞凋亡指数降低(P<0.05)。结论丁酸钠预处理可以抑制内毒素肝损伤小鼠细胞凋亡,其机制可能与减少氧自由基的生成有关。
Objective To investigate the effect of sodium butyrate preconditioning on apoptosis in endotoxic liver injury mice. Methods Forty eight healthy male Kunming mice were randomly divided into four groups (n = 12 each): normal group, model group, bifendate group and sodium butyrate group. Lipopolysaccharide (10 mg / kg) was intraperitoneally injected into mice to induce endotoxin induced liver injury. Six hours after model establishment, serum ALT and AST activities, MDA content and SOD activity in mice were detected, and TUNEL method was used to detect the apoptosis of mouse liver tissue. Results Compared with model group, the contents of ALT, AST and MDA in sodium butyrate group and bifendate group were significantly decreased (P <0.05), the activity of SOD increased (P <0.05) and the apoptosis index of hepatocytes decreased <0.05). Conclusion Sodium butyrate preconditioning can inhibit the apoptosis of endotoxin-induced liver injury in mice. The mechanism may be related to the reduction of the production of oxygen free radicals.