The inhibition of the p65 pathway prevents the induction of cellular senescence and proinflammatory activation. Quantification and representative images of crystal violet to evaluate the proliferation capacity in (A) mesenchymal stem cells (MSCs) treated with JSH-23, MG-132 and curcumin during the cellular senescence establishment (DNA damage-induced senescence (DDIS) and therapy-induced senescence (TIS)) and (B) MSCs treated with JSH-23, MG-132 and curcumin during the proinflammatory activation (PA). All data represent the mean ± SD of three independent experiments. Nonparametric Kolmogorov–Smirnov test was used to calculate the significance, and it was represented as
p < 0.05 and
p < 0.01. (C) Quantification of senescence-associated β-galactosidase activity in MSCs treated with the pharmacological inhibition of the p65 pathway using JSH-23, MG-132 and curcumin during the cellular establishment (DDIS and TIS). All data represent the mean ± SD of three independent experiments. Nonparametric Kolmogorov–Smirnov test was used to calculate the significance, and it was represented as
p < 0.05 and
p < 0.01. NON-Se: Proliferative or nonsenescent MSCs, Se: Senescent MSCs; TNF-α: MSCs treated with tumor necrosis factor alpha, JSH-23: Senescent (DDIS and TIS) or proinflammatory-activated (TNF-α) MSCs treated with JSH-23, MG-132: Senescent (DDIS and TIS) or proinflammatory activated (TNF-α) MSCs treated with MG-132, Curc.: Senescent (DDIS and TIS) or proinflammatory activated (TNF-α) MSCs treated with curcumin and A.U: arbitrary units.