# In Vitro Antioxidant Effects of Coenzyme Q10 on Cellular Metabolism in Aged Mesenchymal Stem Cells
## 4 Discussion  
Coenzyme Q10 is an essential component of the respiratory chain within the inner mitochondrial membrane, playing a pivotal role in mitochondrial function. It acts as a cofactor for uncoupling proteins and modulates the permeability transition pore, as highlighted by [PERSON] et al. (2021) [10]. Reactive oxygen species are major contributors to mesenchymal stem cell aging, primarily through the activation of the Wnt/\(\beta\)-catenin pathway and disruption of the balance between pro-oxidants and antioxidants [28]. As a potent antioxidant, CoQ10 plays a critical role in mitochondrial respiration, maintaining cellular membrane integrity, and regulating gene expression to mitigate oxidative damage [28; 29; 30; 31]. Evidence of its bioenergetic importance includes studies showing reduced CoQ10 levels and compromised antioxidant defenses in aged animals, leading to heightened oxidative stress [32]. This study explores the impact of CoQ10 on MSC metabolism, demonstrating its capacity to reduce \(\beta\)-galactosidase expression, enhance mitochondrial respiration, and strengthen antioxidant defenses. These effects are mediated by upregulating PPAR\(\gamma\) and CAT gene expression, with pronounced benefits observed in late passage cells. These findings underscore CoQ10's robust antioxidant and protective role in counteracting ROS-driven MSC aging. In the context of aging and stem cell proliferation, a concentration-dependent effect of CoQ10 on MSC viability was observed. Late passage cells exhibited a more favorable response to CoQ10 treatment compared with younger cells. This may be due to differences in mitochondrial function, oxidative stress levels, and gene expression profiles between young and old MSCs. Older cells, with higher baseline oxidative stress, are likely more responsive to CoQ10's antioxidant effects. In contrast, younger cells (P5) are more sensitive to higher CoQ10 concentrations. The effects of CoQ10 on oxygen consumption in MSCs provide valuable insights into its role in mitochondrial function across aging stages. CoQ10 is essential in the mitochondrial respiratory chain, transferring electrons between complexes I (NADH dehydrogenase), II (succinate dehydrogenase), and III (cytochrome bc1 complex). Its reduction in metabolic activity in older cells highlights the need for interventions to restore mitochondrial efficiency [33]. A dose-dependent effect following CoQ10 treatment was observed, with 50 uM being the most effective concentration, enhancing the maximum respiration in late-passage  
Figure 6: Changes in FAME profiles following CoQ10 treatment. Data are presented as the mean \(\pm\) SEM from three independent experiments. Statistical significance is denoted as follows: \({}^{**}\)_p_ < 0.001, \({}^{***}\)_p_ < 0.0001.  
cells, improving mitochondrial efficiency, resilience, and reserve capacity, and restoring SRC (a key indicator of cellular response to energetic stress). Supporting evidence suggests that CoQ10 can reverse mitochondrial dysfunction and reduce ROS production, highlighting its potential to mitigate MSC dysfunction and delay aging [13; 28; 34; 35]. CoQ10 supplementation significantly restored mitochondrial function, decreased ROS and lipid peroxide generation, inhibited lipid droplet accumulation, prevented NLRP9 inflammasome formation, and reduced both interleukin-1\(\upbeta\) release and cell death [36]. However, an increase in leak respiration indicates mild uncoupling or an adaptive response to oxidative stress. This suggests a trade-off between improved metabolic activity and increased mitochondrial stress handling, particularly in younger cells. The effects of CoQ10 on antioxidant gene expression are dose- and age-dependent. In early passage cells (P5), CoQ10 exhibits a strong inhibitory response, with a dose-dependent decrease in PPARy, ACC, SOD, and CAT expression. The pronounced suppression at 50 uM suggests a shift in cellular energy balance.