Objective:This study explored the myocardial protection role of Jujuboside A through an ischemia–hypoxia–reperfusion(IHR)model.Materials and Methods:H9c2 cells were induced by D-galactose(D-gal)and IHR to establish ...Objective:This study explored the myocardial protection role of Jujuboside A through an ischemia–hypoxia–reperfusion(IHR)model.Materials and Methods:H9c2 cells were induced by D-galactose(D-gal)and IHR to establish an aging and IHR model.There are four groups of experiments:Control,IHR,D-gal+IHR,and D-gal+IHR+Jujuboside A.Cells viability,Adenosine triphosphate(ATP),reactive oxygen species(ROS),nicotinamide adenine dinucleotide(NAD+),nicotinamide adenine dinucleotide hydride(NADH)content,and NAD+/NADH ratio were detected using biochemical methods.Inflammatory cytokines level was detected by enzyme-linked immunosorbent assay.The expression of CD38,Recombinant NLR Family,pyrin domain-containing protein 3(NLRP3),and silent mating type information regulation 2homolog 3(SIRT3)protein was detected by Western blotting.Results:Compared to the IHR group,cell viability,ATP content,NAD+content,NAD+/NADH ratio,and SIRT3 protein expression decreased,ROS level and inflammatory cytokines increased,and CD38 and NLRP3 proteins raised in the D-gal+IHR group.Compared to the D-gal+IHR group,cell viability,ATP content,NAD+content,NAD+/NADH ratio,and expression of SIRT3 protein increased,ROS level and inflammatory cytokines level decreased,and expression of the CD38 and NLRP3proteins decreased in the D-gal+IHR+Jujuboside A group.Conclusions:Jujuboside A inhibited the expression of CD38,improved energy metabolism disorder,and mitochondrial function,and decreased inflammation in D-gal-induced H9c2 cells.展开更多
基金Construction of atrial fibrillation-specific disease database(shdc2020cr6012-003)3 years action plan of Shanghai Shenkang Medical Development Center(shdc2020cr1053b)+1 种基金Science and technology support project of Shanghai Municipal Commission of Science and Technology(18401932800)Shanghai Shenkang medical development center emerging frontier technology joint research project(shdc12018125)。
文摘Objective:This study explored the myocardial protection role of Jujuboside A through an ischemia–hypoxia–reperfusion(IHR)model.Materials and Methods:H9c2 cells were induced by D-galactose(D-gal)and IHR to establish an aging and IHR model.There are four groups of experiments:Control,IHR,D-gal+IHR,and D-gal+IHR+Jujuboside A.Cells viability,Adenosine triphosphate(ATP),reactive oxygen species(ROS),nicotinamide adenine dinucleotide(NAD+),nicotinamide adenine dinucleotide hydride(NADH)content,and NAD+/NADH ratio were detected using biochemical methods.Inflammatory cytokines level was detected by enzyme-linked immunosorbent assay.The expression of CD38,Recombinant NLR Family,pyrin domain-containing protein 3(NLRP3),and silent mating type information regulation 2homolog 3(SIRT3)protein was detected by Western blotting.Results:Compared to the IHR group,cell viability,ATP content,NAD+content,NAD+/NADH ratio,and SIRT3 protein expression decreased,ROS level and inflammatory cytokines increased,and CD38 and NLRP3 proteins raised in the D-gal+IHR group.Compared to the D-gal+IHR group,cell viability,ATP content,NAD+content,NAD+/NADH ratio,and expression of SIRT3 protein increased,ROS level and inflammatory cytokines level decreased,and expression of the CD38 and NLRP3proteins decreased in the D-gal+IHR+Jujuboside A group.Conclusions:Jujuboside A inhibited the expression of CD38,improved energy metabolism disorder,and mitochondrial function,and decreased inflammation in D-gal-induced H9c2 cells.
