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Abstract To explore the effect of small molecule mediated P38 MAPK signaling pathway inhibition on functional characteristics of UC-MSC. Methods: The 5th generation UC-MSCs were treated with P38 MAPK pathway inhibitor SB202190 in vitro for 48h， and the cell morphology of UC-MSC was observed by microscope. After 48 hours of culture in vitro, cells were digested with 0.25% trypsin, the expression of UC-MSC surface markers was tested by flow cytometry, and the stemness before and after induction of adipogenic differentiation was detected by adipogenesis induced differentiation experiment. Intervention on the back wounds of diabetic rats was implemented to evaluate the effect of P38 MAPK pathway inhibition in UC-MSCs on improving the repair of back skin lesions in diabetic rats. Results: Under the microscope, UC-MSC treated with SB202190 for 48h showed a typical long spindle shape. In addition, the population of cells doubling time was 36h, which had no significant different from that of untreated cells. Flow cytometry showed that positive markers, including CD105, CD73, and CD90, accounted for more than 95% of total UC-MSC surface markers, while the negative markers CD45, CD34, CD14, CD19, and HLA-DR accounted for less than 2%, in both SB202190 treated and untreated cells. In vitro differentiation experiment, inhibition of P38 MAPK pathway in UC-MSC showed red lipid droplets on the 21th day after induction using oil red O staining. Inhibition of P38 MAPK pathway in UC-MSC effectively promoted wound healing of damaged back skin of diabetic rats. On the third day of subcutaneous intervention, wound healing was better than that of UC-MSC without inhibition of the P38 MAPK pathway and PBS. Conclusion: Short-term inhibition of P38 MAPK pathway can effectively enhance tissue repair ability, while have no effect on the phenotype and differentiation of UC-MSC.
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