Nanoparticles–SIRT1 Prevents Endothelial Progenitor Cells Senescence by Modulating Nitric Oxide Expression and Reducing Poly ADP-ribose Polymerase: In vitro Study

One of cardiovascular diseases that accounts for a high global death rate is atherosclerosis. Apart from the known risk factors, the cause of this disease is uncertain. This disease is triggered by the rupture of atheroma. This condition is associated with oxidative stress, which can trigger endothelial progenitor cells (EPC) dysfunction. One of the causes of oxidative stress is hydrogen peroxide, which triggers deoxyribose nucleotide acid (DNA) damage, which will later trigger ageing in EPC. Sirtuin-1 (SIRT1) is known to be involved in EPC repair, but currently, no studies have attempted to increase SIRT1 expression in vitro. This study aimed to determine the effect of nanoparticles-SIRT1 (NPS1) on the expression of nitric-oxide (NO) and poly (ADP-ribose)-polymerase (PARP) in EPC cell cultures induced by hydrogen peroxide (H₂O₂). Tests were carried out in vitro using EPC cell cultures to determine the potential of SIRT1 (NPS1) nanoparticles as an ageing inhibitor. The research method used was pure quantitative experimental with a post-test-only control group. The expression of NO and PARP was studied using the flow cytometry method. The data obtained were analysed using parametric one-way ANOVA and post-hoc Tukey-HSD tests with a 95 % confidence interval (p ≤ 0.05). The results showed that administration of SIRT1 nanoparticles was able to increase NO expression in EPC culture cells that induced H₂O₂ by 14.61 % and could also increase NO levels in normal EPC cells that were only given NPS1 by 38.51 % and was able to reduce PARP expression when compared with the normal group. The NPS1 given was 9.03 % for the NPS1 group and 19.78 % for the NPS1+ H₂O₂ group. This study concludes that NPS1 added to EPC cells further helps increase cell repair to prevent senescence, through increasing NO and also increasing the performance of PARP.