四联活菌制剂Bornlisy对小鼠酒精性肝损伤的保护作用研究

Protective Effect of Bornlisy on Murine Alcoholic-induced Liver Injury and Mechanisms Exploring

摘要:

本研究采用不同浓度乙醇灌胃的方法建立急、慢性酒精性肝损伤模型，观察四联活菌试剂Bornlisy（BO）及其上清对小鼠酒精性肝损伤的保护作用。结果表明，BO可显著提高急性酒精性肝损伤小鼠的生存率（p<0.05），BO上清则无上述效果；在慢性酒精性肝损伤模型中，BO可有效降低慢性酒精性肝损伤引起的肝脏指数升高（p<0.05），改善肝组织脂肪性病变和脂滴蓄存，血清中ALT和TG水平显著降低（p<0.05），肝脏SOD活力显著上升了43.30%（p<0.05），GSH-Px活力明显上升了281.44%（p<0.01），BO上清则无明确疗效；进一步分析脂肪酸代谢信号通路，发现BO可显著抑制过氧化物酶体增殖剂激活受体α（PPARα）、过氧化物酶酰基辅酶A氧化酶（ACOX1）和肝脏脂肪酸结合蛋白（L-FABP）mRNA水平的降低（p<0.05），而BO上清对于PPARα、ACOX1的mRNA水平无显著影响（p>0.05）。对固醇调节元件结合蛋白（SREBP-1c）通路检测，结果显示BO和BO上清均对SREBP-1c和脂肪酸合成酶（FAS）mRNA表达水平无显著性影响。因此，BO对小鼠酒精性肝损伤具有保护作用，这可能是通过抗氧化应激、选择性增强PPARα通路来实现。

Abstract:

In order to investigate the protective effect of probiotics compound preparations Bornlisy (BO) on murine alcoholic-induced liver injury and explore the underlying mechanisms, acute and chronic alcoholic liver injuries models were establishedin mice by gavage with different concentrations of liquor. Compared with the model group, the survival rate of acute alcoholic liver injury mice with BO treatment was significantly improved (p<0.05), while there was no such effect in BO supernatant treatment group. In chronic alcoholic liver injury model, BO could significantly reduce the increase of liver index and improve fatty pathological injuries and lipid accumulation (p<0.05). Levels of serum ALT and TG decreased significantly (p<0.05), and the activity of liver SOD and GSH-Px increased significantly by 43.30%(p<0.05) and 281.44% in BO treatment group (p<0.01), respectively, while BO supernatant treatment group had no certain effects. Through investigating the fatty acid metabolic pathways, we found that BO treatment could inhibit the decrease of mRNA levels of PPARα, ACOX1 and L-FABP significantly (p<0.05), while BO supernatant treatment had no significant effects (p>0.05). The detection results of SREBP-1c pathway showed that both BO and BO supernatant treatment had no significant effects on SREBP-1c and FAS mRNA expressions. Therefore, BO can protect mice from alcoholic induced liver injuries, which may be achieved by anti-oxidative stress and selectively enhancing PPARα pathway.