金银花多糖对BCG+LPS致小鼠免疫性肝损伤的保护作用

Protective Effects of FLP-3 on Immunological Liver Injury Induced by BCG+LPS in Mice

目的:探讨金银花多糖(FLP-3)对卡介苗加脂多糖(BCG+LPS)致小鼠免疫性肝损伤的影响。方法:将72只昆明种小鼠按随机数字表法分为正常组、BCG+LPS免疫性肝损伤小鼠组(模型组)、对照组(联苯双酯)及FLP-3低、中、高剂量组,每组12只;制备小鼠免疫性肝损伤模型;观察各组小鼠肝组织Bcl-2、Bax阳性表达率、血清白细胞介素10(IL-10)、白细胞介素12(IL-12)水平和小鼠肝组织的病理改变。结果:与正常组比较,模型组小鼠肝组织Bax表达上升(P<0.01),Bcl-2表达降低(P<0.01);与模型组比较,FLP-3各剂量组Bax表达下降(P<0.01),Bcl-2表达上升(P<0.01),而FLP-3高剂量组与对照组肝组织Bax及Bcl-2表达比较差异无统计学意义(P>0.05)。与正常组比较,模型组小鼠血清IL-10、IL-12水平升高(P<0.01);与模型组比较,FLP-3各剂量组IL-10、IL-12水平下降(P<0.01);与对照组比较,除FLP-3高剂量组血清IL-12水平差异无统计学意义外,其余剂量组血清IL-10、IL-12水平均降低(P <0.05)。结论:金银花多糖对LPS+BCG致小鼠免疫性肝损伤有明显的保护作用,而防止肝细胞过度凋亡可能是其防治免疫性肝损伤的作用机制。

Objective: To discuss the effects of honeysuckle flos lonicera polysaccharide (FLP-3) on immuno - logical liver injury(ILI) induced by BCG+LPS in mice. Methods: All 72 mice were divided into six groups according to random number table method, that is, the normal group, BCG+LPS-induced ILI group (the model group), the control group (bifendate), low, moderate and high doses groups of FLP-3 12 mice each group;mice models suffering ILI were prepared;to observe pathological changes of liver tissue, the levels of IL-10 and IL-12, positive expression rates of Bcl-2 and Bax. Results: Compared with the normal group, the expressions of Bax in liver tissue of the model group rose (P<0.01), the expression of Bcl-2 decreased (P<0.01);compared with the model group, the expressions of Bax lowered in different doses groups of FLP-3 (P<0.01), the expression of Bcl-2 rose (P<0.01), while there was no significant difference in the comparisons of the expression of Bax and Bcl-2 when high dose group of FLP-3 was compared with the control group (P>0.05). Compared with the normal group, the levels of IL-10 and IL-12 rose in the model group (P<0.01);compared with the model group, the levels of IL-10 and IL-12 lowered in different doses groups of FLP-3 (P<0.01);compared with the control group, the levels of IL-10 and IL-12 lowered in different doses groups except there was no statistical difference in the level of IL-12 in high dose group of FLP-3 (P<0.05). Conclusion: FLP-3 could protect the mice with BCG+LPS - induced ILI obviously, and preventing theexcessive apoptosis of liver cells might be the mechanismof FLP-3 preventing and treating ILI.