Retraction notice to “Echinacoside improves diabetic liver injury by regulating the AMPK/SIRT1 signaling pathway in db/db mice” [Life Sci. 271 (2021) 119237]

Yang, Lifang; Zhang, Xiang; Liao, Min; Hao, Yarong

doi:10.1016/j.lfs.2022.120530

Cited by 1 publication

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“…It exhibits antioxidant, anti‐inflammatory, neuroprotective, hepatoprotective, nitric oxide free radical‐scavenging, and vasodilatory effects. [ 16–21 ] Ech has been proven to have the potential to both prevent and treat a variety of liver diseases, and it has been found that Ech prevents a variety of liver injuries and also has a favorable hepatoprotective effect. [ 22–24 ] Ech increased the activity of nuclear factor erythroid 2‐related factor 2 (Nrf2), which protects against ethanol‐induced liver injury by inhibiting oxidative stress and cell apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Echinacoside Exerts Antihepatic Fibrosis Effects in High‐Fat Mice Model by Modulating the ACVR2A‐Smad Pathway

Liang,

Chen,

et al. 2024

Molecular Nutrition Food Res

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ScopeNonalcoholic steatohepatitis (NASH) is an increasingly common chronic liver disease in which hepatic fibrosis is the major pathological change. The transforming growth factor β (TGF‐β)/mall mothers against decapentaplegic (Smad) signaling is the main effector of fibrosis. Although the antifibrotic effect of echinacoside (Ech) on the liver has been indicated previously, the cellular and molecular mechanisms remain unclear. This study aims to investigate both in vivo and in vitro antifibrotic properties of Ech.Methods and resultsCell viability and scratch/wound assays show that Ech significantly inhibits the proliferation, migration, and activation of human hepatic stellate LX‐2 cells. In mice with high‐fat diet‐induced hepatic fibrosis, Ech treatment attenuates the progression of liver injury, inflammation, and fibrosis. Furthermore, transcriptome analysis and subsequent functional validation demonstrate that Ech achieves antifibrotic effects by the activin receptor type‐2A (ACVR2A)‐mediated TGF‐β1/Smad signaling pathway; ultimately, ACVR2A is demonstrated to be an important target for hepatic fibrosis by inhibiting and inducing the expression of ACVR2A in LX‐2 cells.ConclusionEch exerts potent antifibrotic effects by inhibiting the ACVR2A‐mediated TGF‐β1/Smad signaling axis and may serve as an alternative treatment for hepatic fibrosis.

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Section: Introductionmentioning

confidence: 99%