Fig. 4
The RAS/ERK, PI3K/Akt, and NF-κB/IL-10 pathways are the downstream targets of LPAR1/S1PR1/3-mediated stem cell protection. a Representative images of Western blot results for RAS, phosphorylated ERK (p-ERK), total ERK, phosphorylated PI3K (p-PI3K), total PI3K, phosphorylated Akt (p-Akt), total Akt, and their quantitative data after LPS/H2O2 intoxification, in the presence or absence of LPA/S1P co-treatments (n = 3). b Changes in cell viability and caspase-3/7 activity of hADMSCs after LPS/H2O2 and LPA/S1P treatments, with or without the co-administration of salirasib (RAS inhibitor), UO126 (ERK inhibitor), wortmannin (PI3K inhibitor), or MK2206 (Akt inhibitor) (n = 4). c Changes in nuclear translocation and activation of NF-κB p65 subunit after LPS/H2O2 and LPA/S1P treatments (n = 3). d (left) Changes in IL-10 secretion of hADMSC LPS/H2O2 and LPA/S1P treatments, with or without the co-administration of NF-κB p65 inhibitor anacardic acid (AnaAcid); (right) changes in cell viability after LPS/H2O2/LPA/S1P treatments, with or without IL-10 shRNA co-transfection (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 < 0.01 versus control group; ***p < 0.001 versus control group; ##p < 0.01 versus LPS/H2O2 group; ###p < 0.001 versus LPS/H2O2 group; @@@p < 0.001 versus LPS/H2O2 + LPA or S1P group. Ctrl, control; IL, interleukin; LPA, lysophosphatidic acid; LPS, lipopolysaccharides; S1P, sphingosine-1-phosphate