cPLA2α on the influence of Th17 and its role in the formation of liver fibrosis.

Abstract

This study primarily investigated the mechanism and pathways of the cPLA₂α signaling pathway on Th17-mediated HSC activation and liver fibrosis, providing insights for clinical strategies to target HSC activation and delay the rapid progression of liver fibrosis. In vitro and in vivo model were established, and different concentrations of the cPLA₂α inhibitor AACOCF3 were administered respectively for intervention. The expression of IL- 17 was detected by ELISA, and the expression of cPLA₂α protein and HSC activation protein α-SMA index were detected by Western blot and immunofluorescence. In addition, observe the changes in the degree of liver fibrosis in mice through the pathological staining of mouse livers. In an in vitro system, Th17 could induce HSC activation. And after intervention, the results showed that the inhibitor could inhibit Th17 activation of HSC. Next, in an in vivo model, Th17 could also induce HSC activation. And after intervention, the results showed that the inhibitor could also inhibit HSC activation by Th17. Observation under liver pathological staining showed that the inflammation and staining were significantly reduced in the intervention group, suggesting a therapeutic effect of AACOCF3. Using in vitro and in vivo approaches, these data suggest that Th17 cells can promote the activation and proliferation of HSCs, which further exerts a role in promoting liver fibrosis. These data also suggest that the cPLA₂α pathway may be involved in the activation of HSCs by Th17 cells and induce liver fibrosis mechanisms.