Rapamycin enhanced Autophagy Inhibits Inflammation via Down-Regulation of p38 MAPK/mTOR Signaling

Results: Induction of autophagy with Rapamycin (RAPA) decreased expression levels of IL6, IL8 and CCL20, in addition to reduction in inflammation-induced apoptosis in HUVECs. Moreover, RAPA increased LC3II, while decreasing p62 expression. Likewise, expression levels of p-p38 MAPK and p-mTOR proteins were markedly decreased by the treatment with RAPA. Finally, RAPA treatment increased the NO content and the NOS activity, and inhibited angiogenesis.

Conclusion

In this study, we established a psoriatic endothelial cell model to investigate the effects of autophagy on inflammation and apoptosis of HUVEC. Induction of autophagy can inhibit inflammation and apoptosis, while improving endothelial cell functions in HUVECs treated with M5 cytokines, mediated in part by p38 MAPK/mTOR signaling pathway. Induction of autophagy can improve the function of endothelial cells in psoriasis, potentiating the utility of approaches to enhance autophagy in the treatment of psoriasis.

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