Fig. 2

LPA and/or S1P attenuates LPS/H2O2-induced stem cell oxidative stress and inflammation. a Representative immunofluorescent image and corresponding quantified data (n = 4) of hADMSCs after LPS/H₂O₂ intoxification in the presence or absence of LPA/S1P co-treatments (green: DMPO-stained signal; blue: Hoechst 33,342 counter-stained signal). Scale bar = 50 μm. b Cellular GSH/GSSG ratio (n = 4), c cell endogenous antioxidant enzymes (CAT and SOD1) protein level with quantified data (n = 3), d cell-secreted TNF-α protein level (n = 4), and e cell-secreted IL-6 protein level changes in hADMSCs after LPS/H₂O₂ intoxification in the presence or absence of LPA/S1P co-treatments (n = 4). Data from each group are expressed as means ± SEM. Statistical comparison between groups was performed with the Kruskal–Wallis test followed by Dunn’s post-hoc test to detect differences in all groups. ***p < 0.001 versus control group; ^#p < 0.05 versus LPS/H₂O₂ group; ^##p < 0.01 versus LPS/H₂O₂ group; ^###p < 0.001 versus LPS/H₂O₂ group; ^@@p < 0.01 versus LPS/H₂O₂ + LPA or S1P group; ^@@@p < 0.001 versus LPS/H₂O₂ + LPA or S1P group. CAT, catalase; Ctrl, control; DMPO, 5,5-dimethyl-1-pyrroline-N-oxide; GSH, reduced glutathione; GSSG, oxidized glutathione; IL, interleukin; LPA, lysophosphatidic acid; LPS, lipopolysaccharide; S1P, sphingosine-1-phosphate; SOD1, superoxide dismutase 1; TNF, tumour necrosis factor