Salvianolic acid B(Sal B)is a polyphenolic antioxidant that has been shown to have anti-lipid accumulation,anti-inflammatory,and free oxygen radical scavenging activities in various diseases.Here,we aimed to examine w...Salvianolic acid B(Sal B)is a polyphenolic antioxidant that has been shown to have anti-lipid accumulation,anti-inflammatory,and free oxygen radical scavenging activities in various diseases.Here,we aimed to examine whether Sal B could alleviate non-alcoholic fatty liver disease(NAFLD)and explore the possible mechanisms.Signaling pathways involved in oxidative stress,including SIRT3,SOD2,and FOXO1 pathways,were investigated by Western blotting analysis,RT-qPCR,and immunoprecipitation(IP).In the present study,oleic acid(OA)successfully induced lipid and peroxide accumulation,decreased SIRT3 expression,and increased FOXO1 acetylation.However,Sal B significantly reversed these trends.SIRT3 plasmid transfection further reduced the expression of acetylated FOXO1 and considerably enhanced the regulation of SIRT3 and acetylated FOXO1 induced by Sal B.Following SIRT3 siRNA transfection,Sal B-induced down-regulation of acetylated FOXO1 was blocked,suggesting that Sal B-mediated protection occurred through SIRT3-mediated FOXO1 deacetylation.The SIRT3/FOXO1 pathway was a critical therapeutic target for controlling oxidative stress in NAFLD,and Sal B conferred protection against OA-induced hepatic steatosis and oxidative stress through SIRT3-mediated FOXO1 deacetylation.展开更多
基金supported by grants from Wuhan Municipal Health and Family Planning Commission scientific research project(Grant No.WZ20Z04).
文摘Salvianolic acid B(Sal B)is a polyphenolic antioxidant that has been shown to have anti-lipid accumulation,anti-inflammatory,and free oxygen radical scavenging activities in various diseases.Here,we aimed to examine whether Sal B could alleviate non-alcoholic fatty liver disease(NAFLD)and explore the possible mechanisms.Signaling pathways involved in oxidative stress,including SIRT3,SOD2,and FOXO1 pathways,were investigated by Western blotting analysis,RT-qPCR,and immunoprecipitation(IP).In the present study,oleic acid(OA)successfully induced lipid and peroxide accumulation,decreased SIRT3 expression,and increased FOXO1 acetylation.However,Sal B significantly reversed these trends.SIRT3 plasmid transfection further reduced the expression of acetylated FOXO1 and considerably enhanced the regulation of SIRT3 and acetylated FOXO1 induced by Sal B.Following SIRT3 siRNA transfection,Sal B-induced down-regulation of acetylated FOXO1 was blocked,suggesting that Sal B-mediated protection occurred through SIRT3-mediated FOXO1 deacetylation.The SIRT3/FOXO1 pathway was a critical therapeutic target for controlling oxidative stress in NAFLD,and Sal B conferred protection against OA-induced hepatic steatosis and oxidative stress through SIRT3-mediated FOXO1 deacetylation.
