嗜热链球菌grx02对酒精性肝损伤大鼠保护作用的分子机制

摘要

To study the protection mechanism of Streptococcus thermophilus grx02 on acute alcoholic liver injury in tats .Methods: To establish an acute alcoholic liver injury model and observe the improvement of Streptococcus thermophilus grx02 on the serum aminotransferase and inflam-matory cytokine of acute alcoholic liver injury in rats. Alcohol can induce a remarkable increasement of the levels of rat's serum ALT, AST and MDA- Meanwhile, alcohol can also significantly elevate the levels of tumor necrosis factor —α (TNF—α),inrerleukin —1β (IL—1β), inter-leukin-8 (IL-8)of serum and liver homagerute in rats. However, alcohol can weaken the activity of Alcohol dehydrogenase (ADH), re-ducibility glutathione(GSH), gjutathione peroxidase (GSH-Px)and super oxise dlsmutase (SOD),which are significandy different, compared with the model group.Conclusion: Streptococcus thermophilus grxO2 produces protective effects on acute alcoholic liver injury by inhibiting the growth of inflammatory factors, enhancing the activity of antioxidase system and controlling the formation of liver injury induced by oxidation stress.%研究了嗜热链球菌grx02对急性酒精性肝损伤大鼠模型的保护作用机制.建立了急性酒精性肝损伤大鼠模型,观察嗜热链球菌grx02对急性酒精性肝损伤大鼠血清转氨酶以及炎症细胞因子的改善作用.结果表明、酒精可诱导大鼠血清谷氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、丙二醛(MDA)水平显著升高,；血清、肝匀浆中肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)、白介素-8(IL-8)细胞因子永平显著升高；乙醇脱氢酶(ADH)、还原性谷胱甘肽(GSH)、增加谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性显著下降,与对照组比较均有显著性差异.结论:grx02可能通过抑制炎性因子,增强抗氧化酶系活性、抑制氧化应激引发的肝损伤,对大鼠急性酒精性肝损伤发挥保护作用.