ArticleChinese medicine2026
Therapeutic potential of Sheng-Xian-Tang in doxorubicin-induced chronic heart failure by regulation of phenylalanine metabolism disruption.
Article in Chinese medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Exploring the Mechanism of Zhigancao Decoction in the Treatment of Chronic Heart Failure via Modulation of Oxidative Stress.Rapid communications in mass spectrometry : RCM · 2026Article
- Polyherbal Formulation Attenuates Isoproterenol-Induced Cardiac Toxicity Through Regulation of Mitochondrial Bioenergetics, Lipid Toxicity, and Intrinsic Apoptotic Pathways in Rats.Cell biochemistry and biophysics · 2026Article
- Therapeutic effects of Tetramethylpyrazine on Cartilage in Rat Model of Post-traumatic Osteoarthritis.Regenerative therapy · 2026Article
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Authors and funding
10 authors.
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Abstract
backgroundSheng-Xian-Tang (SXT), a traditional Chinese medicine, ameliorates doxorubicin (DOX)-induced chronic heart failure (CHF), yet its molecular mechanisms remain elusive.
objectiveTo elucidate SXT's cardioprotective mechanisms against DOX-induced CHF.
methodsIn vivo, cardioprotection was evaluated via echocardiography, oxidative stress assays, and histopathology. Integrated metabolomic and 16S rRNA sequencing identified metabolic disruptions. Serum pharmacochemistry analysis identified hepatic bioactive compounds targeting phenylalanine hydroxylase (PAH). Molecular docking, CETSA, SPR, and enzyme activity assay validated neomangiferin-PAH interactions.
resultsSXT dose-dependently improved DOX-induced cardiac dysfunction in rats. Metabolomic and microbiome analyses confirmed phenylalanine metabolic disorder in the CHF rats. DOX exposure elevated phenylalanine levels in plasma, urine, and heart, reducing hepatic PAH expression and function while inducing ectopic phenylalanine catabolism in the heart. Phenylalanine administration exacerbated the cardiac abnormalities, whereas SXT effectively prevented attenuated DOX-induced cardiac toxicity. CETSA and SPR revealed a strong binding of neomangiferin to PAH, stabilizing its interaction with cofactor BH
conclusionsSXT mitigated DOX-induced CHF through hepatic PAH modulation. Neomangiferin could enhance PAH stability via competitive binding. Targeting PAH-phenylalanine metabolism emerged as a novel therapeutic strategy for DOX-induced cardiac dysfunction.
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