原花青素B2通过修复线粒体功能障碍拮抗多柔比星诱导的细胞衰老OA

The protective effects of proanthocyanidin B2(PB2)against doxorubicin(DOX)-induced mitochondrial dysfunction and cellular senescence in human skin fibroblasts(HSFs)was investigated.A DOX-induced HSF senescence model was established,and cells were treated with varying concentrations of PB2.Reactive oxygen species(ROS)levels and mitochondrial membrane potential(ΔΨm)were assessed using fluorescence microscopy.ATP content was measured using commercial assay kits,DNA damage was evaluated via γ-H2AX immunofluorescence,and senescence-associated β-galactosidase(SA-β-gal)staining was used to characterize senescent phenotypes.PB2 treatment effectively mitigated DOX-induced cellular damage.Among the concentrations tested,2 μmol/L PB2 showed the most pronounced effect,reducing intracellular ROS accumulation by over 50%,restoring mitochondrial function(ΔΨm increased 8.75-fold),and enhancing ATP production by 33.08%.Moreover,γ-H2AX expression decreased by 25.53%,and SA-β-gal activity was inhibited by 38.20%.These findings indicate that PB2 delays DOX-induced cellular senescence by scavenging ROS,restoring mitochondrial function(ΔΨm homeostasis and ATP synthesis),and alleviating DNA damage,providing a theoretical basis for the development of PB2-based anti-aging cosmetic products.