ArticleMolecular medicine reports2016
Jia-Shen decoction-medicated serum inhibits angiotensin-II induced cardiac fibroblast proliferation via the TGF-β1/Smad signaling pathway.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Review
- Combined analysis of plasma metabolome and intestinal microbiome sequencing to explore jiashen prescription and its potential role in changing intestine-heart axis and effect on chronic heart failure.Frontiers in cardiovascular medicine · 2023Article
- Based on network pharmacology and in vitro experiments to prove the effective inhibition of myocardial fibrosis by Buyang Huanwu decoction.Bioengineered · 2022Article
- Role of Elevated Thrombospondin-1 in Kainic Acid-Induced Status Epilepticus.Neuroscience bulletin · 2020Article
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8 authors.
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Abstract
Jia-Shen decoction (JSD) is a traditional Chinese medicine, which is used widely to treat chronic heart failure. However, the underlying mechanism remains to be elucidated. The present study aimed to investigate the mechanism underlying the effects of JSD on cardiac fibroblast (CF) proliferation and differentiation. The CFs were obtained from the hearts of neonatal (1‑3‑day old) Sprague‑Dawley rats and treated with JSD-medicated serum (JSDS) with or without angiotensin II (Ang II). Cell proliferation was assessed using Cell Counting Kit‑8 reagent. In addition, the mRNA expression levels of transforming growth factor‑β1 (TGF‑β1) and phosphorylated small mothers against decapentaplegic (p‑Smad)2/3 and their protein expression levels were analyzed. CF proliferation was significantly increased in the Ang II‑treated group, compared with the control group (P<0.05). The expression levels of collagen, α‑smooth muscle actin, TGF‑β1 and p‑Smad2/3 were also increased in the Ang II‑treated group (P<0.05). Following JSDS treatment, the increased levels of collagen and cell proliferation were inhibited, and the increased expression levels of p‑Smad2 and p‑Smad3 were also inhibited (P<0.05). These data suggested that JSDS may inhibit CF proliferation via attenuating the TGF‑β1/Smad signaling pathway.
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