人参皂苷CK抑制内质网应激防治酒精性肝损伤  

Ginsenoside CK inhibits endoplasmic reticulum stress and prevents alcoholic liver injury

作　　者：张宇[1] 王洪波[1] 朱振宇 任辉[1] 蒙轩[2] 刘振文[1] Zhang Yu;Wang Hongbo;Zhu Zhenyu(Dept of Hepatobiliary Surgery of No.302 Hospital of PLA,Beijng 100039)

机构地区：[1]中国人民解放军第302医院肝胆外科,北京100039 [2]中国人民解放军总医院肝胆外科,北京100853

出　　处：《安徽医科大学学报》2019年第5期710-715,共6页Acta Universitatis Medicinalis Anhui

基　　金：国家自然科学基金(编号:81502376);北京市自然科学基金(面上项目)(编号:7172201);北京市科技新星计划(编号:Z181100006218089)

摘　　要：目的探究人参皂苷CK抑制内质网应激调节酒精性肝损伤病理变化、细胞凋亡、超微结构和脂质合成代谢。方法建立大鼠酒精性肝损伤动物模型,造模成功后人参皂苷CK干预处理3周。各组[正常组、模型组、低浓度(20 mg/kg)人参皂苷CK干预组、高浓度(40 mg/kg)人参皂苷CK干预组、腺苷蛋氨酸阳性对照组]肝脏组织HE染色进行病理学检测,Western blot检测各组内质网应激标志蛋白GRP78表达量,Annexin V-FITC/PI双标记法检测肝细胞凋亡,电镜观察各组肝细胞超微结构,检测肝细胞内甘油三酯含量。结果高浓度(40 mg/kg)人参皂苷CK干预明显改善酒精性肝损伤大鼠肝脏组织病理改变,显著降低肝损伤引起的GRP78蛋白表达量升高,有效抑制酒精刺激大鼠肝脏引起的细胞凋亡及线粒体结构损伤,降低甘油三酯含量。结论高浓度(40 mg/kg)人参皂苷CK可以抑制内质网应激反应,影响酒精性肝损伤细胞凋亡、超微结构、脂质合成代谢,在一定程度上抑制酒精性肝病。Objective To investigate the effects of ginsenoside metabolite compound K(ginsenoside CK) on pathological changes,cell apoptosis,ultrastructure and lipid metabolism in alcoholic liver injury through endoplasmic reticulum stress(ERS). Methods After successfully established the rat model of alcoholic liver injury,ginsenoside metabolite compound K was used for intervention for 3 weeks. For normal group,model group,low concentration (20 mg/kg) ginsenoside CK intervention group,high concentration(40 mg/kg) ginsenoside CK intervention group and adenosylmethionine positive control group,HE staining was used to pathological examination of liver tissues,Western blot was used to detect the relative expression of ERS marker protein GRP78,Annexin V-FITC/PI double labeling method was used for detection of hepatocyte apoptosis,electron microscope observation was used for liver cell ultrastructure and triglyceride was measured. Results The intervention of high concentration(40 mg/kg) of ginsenoside CK of alcoholic liver injury model significantly improved the pathological changes of liver tissue,reduced the increased GRP78 protein expression caused by liver injury,effectively inhibited the apoptosis and mitochondrial structure damage induced by alcohol,and reduced the content of triglyceride. Conclusion This study demonstrates that high concentration (40 mg/kg) of ginsenoside CK can inhibit ERS response and effect on cell apoptosis,ultrastructure and lipid metabolism in alcoholic liver injury,and inhibit alcoholic liver disease to a certain extent.

关 键 词：人参皂苷CK 内质网应激 酒精性肝损伤 

分 类 号：R575.3[医药卫生—消化系统]