人参皂苷Re改善高糖高脂诱导的H9C2心肌细胞脂代谢及线粒体功能的研究  

Effect of Ginsenoside Re on lipid metabolism and mitochondrial function of H9C2 cardiomyocytes induced by high glucose and high lipid

作　　者：纪磊[1] 徐冰洁 王华婷 刘盈盈[2] Ji Lei;Xu Bingjie;Wang Huating;Liu Yingying(Department of Cardiology,China-Japan Union Hospital of Jilin University,Changchun 130033,Jilin,China;Department of Nephrology,China-Japan Union Hospital of Jilin University,Changchun 130033,Jilin,China)

机构地区：[1]吉林大学中日联医院心内科,长春130033 [2]吉林大学中日联谊医院肾内科,长春130033

出　　处：《中华老年医学杂志》2025年第4期518-524,共7页Chinese Journal of Geriatrics

基　　金：吉林省自然科学基金(YDZJ20201ZYTS020,YDZJ20201ZYTS107)。

摘　　要：目的探究人参皂苷Re通过调控AMPK、Sp1改善高糖高脂诱导的H9C2心肌细胞脂代谢及线粒体功能的机制。方法采用高糖高脂(high glucose and high lipid,HGHL)诱导的H9C2心肌细胞模型,设立空白对照组(CON组)、模型组(HGHL组)、人参皂苷Re组(Re 60μmol/L组)、模型+人参皂苷Re 20μmol/L组(HGHL+Re 20μmol/L组)、模型+人参皂苷Re 40μmol/L组(HGHL+Re 40μmol/L组)、模型+人参皂苷Re 60μmol/L(HGHL+Re 60μmol/L组)。苏木精-伊红染色观察各组细胞形态,油红O染色观察细胞内油脂情况,荧光试剂盒检测细胞内活性氧水平、TUNEL检测细胞凋亡情况,蛋白免疫印迹法检测细胞内的磷酸化AMP依赖的蛋白激酶(phosphorylated adenosine monophosphate-activated protein kinase,pAMPK)、转录因子特异蛋白1(specificity protein 1,Sp1)、核呼吸因子1(nuclear respiratory factor 1,Nrf1)、过氧化物酶体增殖物激活受体辅助激活因子1α(peroxisome proliferator-activated receptor gamma coactivator 1 alpha,PGC-1α)表达情况。结果与CON组比较,HGHL组细胞明显肥大,活性氧水平明显增加,细胞凋亡明显,细胞内甘油三酯明显增多,pAMPK、Nrf1、PGC-1α表达显著降低,Sp1表达显著增加(P<0.05);与模型组比较,HGHL+Re 20μmol/L组、HGHL+Re 40μmol/L组、HGHL+Re 60μmol/L组细胞肥大改善,活性氧水平明显降低,细胞凋亡减轻,细胞内甘油三酯明显减少,pAMPK、Nrf1、PGC-1α表达显著增加,Sp1表达显著降低,且呈剂量依赖(P<0.05)。结论人参皂苷Re对高糖高脂诱导的H9C2心肌细胞脂代谢及线粒体氧化应激、凋亡具有改善作用,与其调控AMPK、Sp1蛋白,增加pAMPK、Nrf1、PGC-1α表达,降低Sp1的表达有关。Objective To investigate the mechanism through which ginsenoside Re enhances lipid metabolism and mitochondrial function in H9C2 cardiomyocytes induced by high glucose and high fat,specifically by modulating AMP-activated protein kinase(AMPK)and specificity protein 1(Sp1).Methods The H9C2 cardiomyocyte model was cultured in a high-glucose and high-lipid(HGHL)environment.Six groups were established:a control group(CON group),a model group(HGHL group),a ginsenoside Re 60μmol/L group(Re 60μmol/L),a model+ginsenoside Re 20μmol/L group(HGHL+Re 20μmol/L),a model+ginsenoside Re 40μmol/L group(HGHL+Re 40μmol/L),and a model+ginsenoside Re 60μmol/L group(HGHL+Re 60μmol/L).Cell morphology was assessed using hematoxylin and eosin(HE)staining,while intracellular oil and triglyceride content were evaluated using oil red O staining.Reactive oxygen species(ROS)levels were measured with a fluorescence kit,apoptosis was assessed using TUNEL staining,and the expressions of phosphorylated AMPK,Sp1,nuclear respiratory factor 1(Nrf1),and peroxisome proliferator-activated receptor gamma coactivator 1 alpha(PGC1α)were analyzed via Western blotting.Results Compared to the control group,the model group exhibited significant increases in cell hypertrophy,ROS levels,apoptosis,and intracellular TG.Conversely,the expressions of pAMPK,Nrf1,and PGC1αwere significantly decreased,while the expression of Sp1 was significantly increased(P<0.05).Compared to the model group,treatment with Ginsenoside Re at concentrations of 20μmol/L,40μmol/L,and 60μmol/L significantly improved cell hypertrophy,reduced ROS levels,alleviated apoptosis,and decreased intracellular TG levels.Additionally,the expressions of pAMPK,Nrf1,and PGC1αwere significantly increased,while Sp1 expression was significantly decreased in a dose-dependent manner(P<0.05).Conclusions Ginsenoside Re enhances lipid metabolism,mitigates mitochondrial oxidative stress,and reduces apoptosis in H9C2 cardiomyocytes induced by high glucose and high lipid conditions.This effect is asso

关 键 词：人身皂苷类 腺苷酸活化蛋白激酶 转录因子特异蛋白1 心肌 线粒体 氧化应激 凋亡 

分 类 号：R285.5[医药卫生—中药学]