Fig. 4

PLX3397 reduces macrophage senescence via PI3K/AKT/FOXO1 signaling. (A) The periodontitis model in vitro, and all protocols followed the procedure exactly. (B) SA-β-gal activity in RAW264.7 cells, and the proportion of SA-β-gal positive cells across groups; Scale Bar = 100 μm. (C) The protein expression of p16 and p21 in RAW264.7 cells and the values of p16 and p21 levels normalized to β-actin across groups. (D) The mRNA expression of IL-6, IL-1β, and TNF-α relative to GAPDH across groups. (E) The protein expression of p-PI3K, PI3K, p-AKT, AKT, p-FOXO1, FOXO1, p16, p21, and β-actin in RAW264.7 cells and the values of PI3K, AKT and FOXO1 levels relative to β-actin and p-PI3K/PI3K, p-AKT/AKT, and p-FOXO1/FOXO1 across groups. C = control cells, LPS = cells treated with P.g-LPS, M = cells treated with 500 nM PLX3397, and LY = cells treated with 25 µM LY294002. The results are presented as a mean ± standard error; n = 3; comparisons between C vs. LPS, M vs. LPS, and LY vs. LPS by one-way ANOVA; *p < 0.05, **p < 0.01, and ***p < 0.001.