发酵乳杆菌KP101对棕榈酸诱导的HepG2肝细胞脂质积累的改善机制  

Mechanism of Lactobacillus fermentum KP101 on improving palmitic acid-induced lipid accumulation in HepG2 liver cells

作　　者：王朝[1,3,4] 王秀娟[1,3,4] 南博[1,3,4] 王宇 李侠[1,3,4] 王玉华[1,3,4] 朴春红 WANG Chao;WANG Xiujuan;NAN Bo;WANG Yu;LI Xia;WANG Yuhua;PIAO Chunhong(College of Food Science and Engineering,Jilin Agricultural University,Changchun Jilin 130118,China;School of Food and Pharmaceutical Engineering/Guangxi Liubao Tea Modern Industry College,Wuzhou University,Wuzhou Guangxi 543002,China;Food Biomanufacturing Science and Technology Innovation Center,Jilin Agricultural University,Changchun Jilin 130118,China;National Processing Laboratory for Soybean Industry and Technology,Jilin Agricultural University,Changchun Jilin 130118,China)

机构地区：[1]吉林农业大学食品科学与工程学院,吉林长春130118 [2]梧州学院食品与制药工程学院/六堡茶现代产业学院,广西梧州543002 [3]吉林农业大学食品生物制造科技创新中心,吉林长春130118 [4]吉林农业大学大豆工业与技术国家加工实验室,吉林长春130118

出　　处：《延边大学农学学报》2025年第1期72-86,共15页Journal of Agricultural Science Yanbian University

基　　金：辅助降血脂功能性乳酸菌筛选及食品开发研究(20230402032GH)。

摘　　要：该研究构建了体外HepG2细胞模型,以评估发酵乳杆菌KP101对棕榈酸(palmitic acid,PA)诱导的HepG2肝细胞脂质代谢紊乱的改善效果及其作用机制。试验结果表明:发酵乳杆菌KP101显著降低了PA诱导的HepG2细胞中总胆固醇(total cholesterol,TC)、甘油三酯(triglyceride,TG)和低密度脂蛋白(low-density lipoprotein,LDL)水平,并提升了高密度脂蛋白(high-density lipoprotein,HDL)水平。此外,发酵乳杆菌KP101还降低了细胞外天冬氨酸转氨酶(aspartate aminotransferase,AST)和丙氨酸转氨酶(alanine aminotransferase,ALT)的浓度。同时,发酵乳杆菌KP101增强了细胞内的超氧化物歧化酶(superoxide dismutase,SOD)和过氧化氢酶(catalase,CAT)活性,减少了丙二醛(malondialdehyde,MDA)积累,从而缓解了因脂质代谢紊乱引发的氧化应激反应。通过检测与脂质代谢相关基因表达水平发现,发酵乳杆菌KP101下调了脂肪酸合成酶(fatty acid synthase,FAS)和固醇调节元件结合蛋白1c(sterol regulatory element binding proteins 1c,SREBP-1c)等脂质合成基因表达,同时上调了过氧化物酶体增殖物激活受体α(peroxisome proliferator-activated receptor alpha,PPAR-α)、脂肪甘油三酯脂肪酶(adipose triglyceride lipase,ATGL)和过氧化物酶体增殖物激活受体γ辅激活因子1α(peroxisome proliferatoractivated receptor gamma coactivator 1-alpha,PGC-1α)等促进脂质分解的基因表达,进而调节脂质代谢。该研究为发酵乳杆菌KP101改善细胞脂质积累提供了重要的数据支持。This study established an in vitro HepG2 cell model to evaluate the improvement effect and mechanism of Lactobacillus fermentum KP101 on lipid metabolism disorder in HepG2 liver cells induced by palmitic acid(PA).The experimental results showed that L.fermentum KP101 could significantly reduce the levels of total cholesterol(TC),triglyceride(TG),and low-density lipoprotein(LDL)in PA-induced HepG2 cells,and increase the level of high-density lipoprotein(HDL).In addition,L.fermentum KP101 also decreased the concentrations of aspartate aminotransferase(AST)and alanine aminotransferase(ALT)in the extracellular fluid.Meanwhile,L.fermentum KP101 enhanced the activities of intracellular superoxide dismutase(SOD)and catalase(CAT),and decreased the accumulation of malondialdehyde(MDA),thereby alleviating the oxidative stress response caused by lipid metabolism disorders.By detecting the expression levels of genes related to lipid metabolism,it was found that L.fermentum KP101 downregulated the expression of lipid synthesis genes such as fatty acid synthase(FAS)and sterol regulatory element-binding protein-1c(SREBP-1c),while upregulating the expression of genes promoting lipid decomposition such as peroxisome proliferator-activated receptorα(PPAR-α),adipose triglyceride lipase(ATGL),and peroxisome proliferator-activated receptorγcoactivator 1α(PGC-1α),thereby regulating lipid metabolism.This study provides important data support for L.fermentum KP101 in improving lipid accumulation in cells.

关 键 词：发酵乳杆菌KP101 HepG2肝细胞 脂质积累 机制研究 

分 类 号：TS201.3[轻工技术与工程—食品科学]