江苏大学学报（医学版）2025，Vol.35Issue(3)：191-196,211,7.DOI:10.13312/j.issn.1671-7783.y240143
丁酸钠激活自噬改善油酸和AGEs诱导的肝细胞脂质沉积和炎症反应
Sodium butyrate activates autophagy to improve oleic acid and AGEs-induced lipid deposition and inflammatory response in hepatocytes
摘要
Abstract
Objective:Investigating the inhibitory effects of sodium butyrate(NaB)on oleic acid(OA)and advanced glycation end-products(AGEs),and exploring its impact and mechanism on lipid deposition and inflammatory response in HepG2 cells.Methods:HepG2 cells were divided into 5 groups:control group(NC),cells without any treatment;OA group,cells treated with 0.05 mmol/L OA for 2 h;OA+AGEs group,cells co-treated with 0.05 mmol/L OA and 200 μg/mL AGEs for 2 h;OA+AGEs+low concentration NaB group(NaB-L),OA+AGEs+high concentration NaB group(NaB-H),where NaB-L group and NaB-H group cells were pre-treated with concentrations of 100 μmol/L and 400 μmol/L NaB for 24 h,then treated with 0.05 mmol/L OA and 200 μg/mL AGEs for 2 h.qRT-PCR was used to detect the mRNA expressions of inflammatory factors,mitochondrial autophagy-related genes,and cholesterol metabolism-related genes.Western blotting was used to detect the expressions of LC3-Ⅱand P62,as well as the distribution of cytochrome C(CytoC)in mitochondria and cytoplasm;flow cytometry was used to detect cellular reactive oxygen species(ROS)and mitochondrial membrane potential levels.Results:Compared to the NC group,lipid deposition in the cells,the NLRP3,Caspase-1,IL-1β,HMGR mRNA,P62,cytoplasmic CytoC expression levels,and ROS levels in the OA+AGEs group were significantly increased(P<0.05),while the LDLR,PINK1,Parkin mRNA expression levels and mitochondrial membrane potential was significantly decreased(P<0.05),as well as the expression levels of CytoC in mitochondria,and LC3-Ⅱ(P<0.05).Compared to the OA+AGEs group,both low and high concentrations of NaB significantly reduced lipid deposition in the cells,the expressions of NLRP3,Caspase-1,IL-1β,HMGR mRNA,P62,cytoplasmic CytoC and ROS levels(P<0.05),while significantly increased the expression of LDLR,PINK1,Parkin mRNA and mitochondrial membrane potential(P<0.05),as well as the expressions of CytoC in mitochondria,LC3-Ⅱ(P<0.05).Conclusion:NaB enhances mitophagy via the PINK1/Parkin pathway,reducing ROS accumulation and CytoC release,thereby suppressing OA/AGEs-induced lipid deposition and inflammatory response.关键词
丁酸钠/晚期糖基化终末产物/非酒精性脂肪性肝病/脂质沉积/炎症反应/线粒体自噬Key words
sodium butyrate/advanced glycosylation end products/non-alcoholic fatty liver disease/lipid deposition/inflammatoion/mitochondrial autophagy分类
临床医学引用本文复制引用
谭家骏,孙文,董雪云,和佳鸳,王平平,吴亮..丁酸钠激活自噬改善油酸和AGEs诱导的肝细胞脂质沉积和炎症反应[J].江苏大学学报（医学版）,2025,35(3):191-196,211,7.基金项目
江苏省中医药科技发展计划项目(MS2022126) （MS2022126）
镇江市科技创新资金(重点研发计划—社会发展)项目(SH2023073) （重点研发计划—社会发展）
