CD38 Deficiency Protects the Heart from Ischemia/Reperfusion Injury through Activating SIRT1/FOXOs-Mediated Antioxidative Stress Pathway
Knockdown of CD38 protects the myocardial cells from hypoxia/reoxygenation- (H/R-) induced death in H9c2 cells. (a) Relative mRNA expressions of CD38 in wild type and CD38 knockdown H9c2 cells. The mRNA expressions of CD38 were determined by real-time PCR and the expression of CD38 was reduced to 5% after gene silence was induced in H9c2 cells. (b) Survival rates of H9c2 cells after 4 h of hypoxia followed different times of reoxygenation. The cell viabilities were examined by CCK8 assay. Although the cell viability of both CD38 knockdown and WT cells was decreased when the cells were treated with H/R, the viability of the myocardial cells in CD38 knockdown cells was much higher than that of WT cells. (c) LDH release in the supernatant of the cell culture after H/R stimulation. The LDH release of CD38 knockdown cells was significantly reduced compared with the normal H9c2 cells. (d) Quantitative analysis of cell apoptosis after H/R stimulation. The apoptosis of myocardial cells was detected with Annexin V-PI staining. The cell apoptosis was attenuated in CD38 gene silenced cells (26.67% ± 0.8969) compared with control cells (19.07% ± 0.7535, , and and ; NS: no significance).
Article of the Year Award: Outstanding research contributions of 2020, as selected by our Chief Editors. Read the winning articles.