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Article Publish Status: FREE
Abstract Title:

Liquiritigenin suppresses the activation of hepatic stellate cells via targeting miR-181b/PTEN axis.

Abstract Source:

Phytomedicine. 2020 Jan ;66:153108. Epub 2019 Oct 4. PMID: 31790896

Abstract Author(s):

Wujun Geng, Guangyao Zhou, Binyu Zhao, Qingqing Xiao, Chunxue Li, Sinuo Fan, Peihong Dong, Jianjian Zheng

Article Affiliation:

Wujun Geng

Abstract:

BACKGROUND: Liquiritigenin (LQ), an aglycone of liquiritin in licorice, has demonstrated antioxidant, anti-inflammatory and anti-tumor activities. Previously, LQ was found to inhibit liver fibrosis progression.

PURPOSE: Phosphatase and tensin homolog (PTEN) has been reported to act as a negative regulator of hepatic stellate cell (HSC) activation. However, the roles of PTEN in the effects of LQ on liver fibrosis have not been identified to date.

METHODS: The effects of LQ on liver fibrosis in carbon tetrachloride (CCl) mice as well as primary HSCs were examined. Moreover, the roles of PTEN and microRNA-181b (miR-181b) in the effects of LQ on liver fibrosis were examined.

RESULTS: LQ markedly ameliorated CCl-induced liver fibrosis, with a reduction in collagen deposition as well asα-SMA level. Moreover, LQ induced an increase in PTEN and effectively inhibited HSC activation including cell proliferation, α-SMA and collagen expression, which was similar with curcumin (a positive control). Notably, loss of PTEN blocked down the effects of LQ on HSC activation. PTEN was confirmed as a target of miR-181b and miR-181b-mediated PTEN was involved in the effects of LQ on liver fibrosis. LQ led to a significant reduction in miR-181b expression. LQ-inhibited HSC activation could be restored by over-expression of miR-181b. Further studies demonstrated that LQ down-regulated miR-181b level via Sp1. Collectively, we demonstrate that LQ inhibits liver fibrosis, at least in part, via regulation of miR-181b and PTEN.

CONCLUSION: LQ down-regulates miR-181b level, leading to the restoration of PTEN expression, which contributes to the suppression of HSC activation. LQ may be a potential candidate drug against liver fibrosis.

Study Type : In Vitro Study

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Sayer Ji
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