Jujuboside a improved energy metabolism in senescent H9c2 cells injured by ischemia, hypoxia, and reperfusion through the CD38/Silent mating type information regulation 2 homolog 3 signaling pathway

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 2 homolog 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 NLRP3 proteins 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.