Frontiers in pharmacology · 2026
Cerevisterol from Ophiocordyceps sinensis fruiting bodies against liver fibrosis.
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Yang Minting, Sun Tao, Han Richou, Xie Huichun, Cao Li
Аннотация
OBJECTIVE: Liver fibrosis is a critical pathological process to irreversible cirrhosis. The valued Ophiocordyceps sinensis (Berk.) G.H. Sung, J.M. Sung, Hywel-Jones and Spatafora (Ophiocordycipitaceae, Hypocreales) fungus exhibits remarkable hepatoprotective effects, especially anti-inflammation. However, detailed metabolites with anti-inflammation activity need to be explored from this fungus. This study investigates the anti-liver fibrosis effect of cerevisterol extracted from O. sinensis fruiting bodies on TGF-β1-induced LX-2 cells (a human hepatic stellate cell line) and the underlying potential mechanisms.
METHODS: The metabolites were extracted and purified by petroleum ether, ethanol reflux extraction and chromatographic separation technology. Their structures were identified based on extensive NMR and MS data. TGF-β1-induced LX-2 cells were employed to study the anti-inflammation activity of the isolated cerevisterol. The mRNA expression of Smad3, Smad4, and Collagen I in the cells was verified by qRT-PCR and Smad3 and Smad4 proteins by Western blot.
RESULTS: Cerevisterol, adenosine, uridine, ergosterol, 2-piperidone, L-tryptophan and (24S)-ergost-7(8)-en-3β,5α,6β-triol were obtained. In the TGF-β1-induced fibrosis model, cerevisterol (10 μM) and a commercial anti-liver fibrosis drug containing Chinese cordyceps (75 ng/mL) as positive control significantly suppressed cell proliferation at 72 and 96 hours. qRT-PCR analysis demonstrated that cerevisterol downregulated mRNA expression of Smad3, Smad4, and Collagen I. Western blot results confirmed reduced protein levels of Smad3 and Smad4 in the cerevisterol-treated cells.
DISCUSSION: Cerevisterol from O. sinensis fungus exerts anti-liver fibrosis effects by inhibiting hepatic stellate cell activation and proliferation, and by downregulating TGF-β/Smad3 signaling pathway, thereby reducing excessive extracellular matrix-related gene and protein expression.
METHODS: The metabolites were extracted and purified by petroleum ether, ethanol reflux extraction and chromatographic separation technology. Their structures were identified based on extensive NMR and MS data. TGF-β1-induced LX-2 cells were employed to study the anti-inflammation activity of the isolated cerevisterol. The mRNA expression of Smad3, Smad4, and Collagen I in the cells was verified by qRT-PCR and Smad3 and Smad4 proteins by Western blot.
RESULTS: Cerevisterol, adenosine, uridine, ergosterol, 2-piperidone, L-tryptophan and (24S)-ergost-7(8)-en-3β,5α,6β-triol were obtained. In the TGF-β1-induced fibrosis model, cerevisterol (10 μM) and a commercial anti-liver fibrosis drug containing Chinese cordyceps (75 ng/mL) as positive control significantly suppressed cell proliferation at 72 and 96 hours. qRT-PCR analysis demonstrated that cerevisterol downregulated mRNA expression of Smad3, Smad4, and Collagen I. Western blot results confirmed reduced protein levels of Smad3 and Smad4 in the cerevisterol-treated cells.
DISCUSSION: Cerevisterol from O. sinensis fungus exerts anti-liver fibrosis effects by inhibiting hepatic stellate cell activation and proliferation, and by downregulating TGF-β/Smad3 signaling pathway, thereby reducing excessive extracellular matrix-related gene and protein expression.