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Icaritin Inhibits Skin Fibrosis through Regulating AMPK and Wnt/β-catenin Signaling

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Abstract

Skin fibrosis is one of the major features of scleroderma. WNT/β-catenin signaling is associated with the progression of skin fibrosis. In this study, we aimed to determine the effect of icaritin (IT), a natural compound, on scleroderma-related skin fibrosis and its mechanisms. We found that IT could reduce the expression of COL1A1, COL1A2, COL3A1, CTGF, and α-SMA in human foreskin fibroblasts (HFF-1 cells), scleroderma skin fibroblasts (SSF cells), and TGF-β-induced HFF-1 cells. Wnt/β-catenin signaling was shown to be suppressed by IT. Additionally, IT activated AMPK signaling in HFF-1 cells. In conclusion, IT has an anti-skin fibrotic effect through activation of AMPK signaling and inhibition of WNT/β-catenin signaling. Our findings indicate the potential role of IT in the treatment of scleroderma and provide novel insight for the selection of drug therapy for scleroderma.

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Acknowledgements

This work is supported by the National Natural Science Foundation of China (Grant no. 81673917), and Fujian provincial health technology project (No. 2016 -ZQN-14).

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Correspondence to Wenyu Wu or Jinfeng Wu.

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Li, M., Liu, Q., He, S. et al. Icaritin Inhibits Skin Fibrosis through Regulating AMPK and Wnt/β-catenin Signaling. Cell Biochem Biophys 79, 231–238 (2021). https://doi.org/10.1007/s12013-020-00952-z

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