Key result
Xanthiumnolic C suppresses myocardial fibrosis markers via inhibiting the TGF-β/Smad signaling pathway.
Why the study?
Although Schisandra sphenanthera fruit exhibits diverse pharmacological properties, its therapeutic potential for myocardial fibrosis remains unexplored.
Does Xanthiumnolic C ameliorate myocardial fibrosis in a TGF-β1-induced cardiac fibroblast cellular model?
Does Xanthiumnolic C ameliorate myocardial fibrosis in a TGF-β1-induced cardiac fibroblast cellular model?
Xanthiumnolic C, derived from Schisandra sphenanthera, exhibits significant antioxidant properties and attenuates TGF-β1-induced myocardial fibrosis in vitro by inhibiting the TGF-β/Smad signaling pathway.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for Xanthiumnolic C in myocardial fibrosis; requires in vivo validation before clinical consideration.
Myocardial fibrosis serves as a fundamental pathology for the pathogenesis and progression of cardiovascular diseases, characterized primarily by excessive proliferation of cardiac fibroblasts and pathological accumulation of extracellular matrix components. Although Schisandra sphenanthera fruit exhibits diverse pharmacological properties, its therapeutic potential for myocardial fibrosis remains unexplored. In this study, a phenylpropanoid compound designated W-23 (Xanthiumnolic C) was isolated from Schisandra sphenanthera. Structural elucidation was achieved through mass spectrometry (MS), nuclear magnetic resonance (NMR) spectroscopy, and carbon spectrum analysis. The antioxidant and antimyocardial fibrosis activities of Xanthiumnolic C were evaluated in vitro. Xanthiumnolic C demonstrated significant antioxidant activity. In a cellular model of myocardial fibrosis, administration of Xanthiumnolic C significantly suppressed the expression of Vimentin (Vim), α-Smooth Muscle Actin (α-SMA), and proteins associated with the TGF-β/Smad signaling pathway, while concurrently downregulating levels of type I and III collagen. Furthermore, Xanthiumnolic C reduced the mRNA expression of Acta2, FN, Col 1 1a1, Vim, MMP-2, and MMP-9. Collectively, these effects ameliorated myocardial fibrosis, suggesting that Xanthiumnolic C holds promise as a potential therapeutic agent for antimyocardial fibrotic drug development.
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Zhang et al. (2026) studied Myocardial fibrosis (in vitro cellular model). Xanthiumnolic C vs. TGF-β1 stimulation alone (model group) and Captopril (positive control) was evaluated on Expression of fibrosis-related proteins (Vimentin, α-SMA, and TGF-β/Smad signaling proteins) (p=<0.05). Xanthiumnolic C significantly suppressed the expression of Vimentin, α-Smooth Muscle Actin, and proteins associated with the TGF-β/Smad signaling pathway in a TGF-β1-induced cellular model of myocardial fibrosis.
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