Effect and mechanism of dental pulp mesenchymal stem cells in inhibiting the inflammatory response of oral lichen planus keratinocytes
Objective To investigate the inhibitory effect and mechanism of dental pulp mesenchymal stem cells on oral lichen planus(OLP)inflammation.Methods Morphological observation and flow cytometry were used to evaluate the properties of human dental pulp mesenchymal stem cells(DP-MSCs)amplified by serum-free medium.The keratinocyte line HaCaT was treated with li-popolysaccharide(LPS)to simulate the OLP inflammation model in vitro.Transwell and DP-MSCs were co-cultured.The effects of DP-MSCs on the proliferation of HaCaT cells were detected by CCK-8 method.The paracrine contents of tumor necrosis factor-α(TNF-α)andinterleukin-6(IL-6)were analyzed by enzyma-linked immunosorbent assay(ELISA).The protein expression of p38 MAPK signaling pathway was detected by Westernblot.Results The isolated DP-MSCs possessed typical morphological character-istics and surface marker molecules of mesenchymal stem cells.Compared with LPS treatment group,the proliferation ability of HaCaT cells significantly increased in the DP-MSCs co-culture group(P<0.05).DP-MSCs co-culture effectively inhibited the paracrine contents of TNF-α and IL-6 in HaCaT cells mediated by LPS(P<0.05).The expression of p-p38 protein in HaCaT cells was sig-nificantly increased after LPS treatment,and co-culture with DP-MSCs significantly inhibited the expression of p-p38 protein(P<0.05).In addition,SB202190,a specific inhibitor of p38 MAPK,worked with DP-MSCs to inhibit the paracrine levels of TNF-α and IL-6 in LPs-stimulated HaCaT cells(P<0.05).Conclusion DP-MSCs can significantly restore the inhibitory effect of LPS on the proliferation of HaCaT cells and down-regulate the paracrine levels of TNF-α and IL-6 by inhibiting p38 MAPK signaling pathway,and reduce the LPS-mediated inflammatory response of HaCaT cells,providing a new therapeutic strategy for oral lichens planus.
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