ArticleZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics2016
[Tranilast inhibits myocardial fibrosis in mice with viral myocarditis].
Article in Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Tranilast reduces cardiomyocyte injury induced by ischemia‑reperfusion via Nrf2/HO‑1/NF‑κB signaling.Experimental and therapeutic medicine · 2023Article
- Cardiac fibrosis: potential therapeutic targets.Translational research : the journal of laboratory and clinical medicine · 2019Review
- Coxsackieviruses B3 infection of myocardial microvascular endothelial cells activates fractalkine via the ERK1/2 signaling pathway.Molecular medicine reports · 2017Article
- Tranilast Can be a Useful Addition to the Limited Anti-Epidermolysis Bullosa Weaponry.Advanced pharmaceutical bulletin · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the effect of tranilast on myocardial fibrosis in mice with viral myocarditis (VMC).
methodsMale balb/c mice (n=72) were randomly divided into control, VMC and tranilast groups (n=24 each). In the VMC and tranilast groups, the mice were infected with Coxsackie virus B3 (CVB3) to prepare VMC model, while the control group was treated with Eagle's medium. After modeling, the tranilast group was administrated with tranilast [200 mg/(kg.d)] until the day before sampling. On days 7, 14 and 28 after CVB3 or Eagle's medium infection, heart specimens (n=8) were taken and examined after Toluidine blue staining and Nissl staining for counts of mast cells (MC), hematoxylin-eosin staining for myocardial pathological changes, and Masson staining for myocardial fibrosis. The expression of CTGF and type I collagen (Col I) in the myocardial tissue was measured by RT-PCR and Western blot. The correlations of CTGF mRNA expression with MC counts and Col I expression were analyzed.
resultsThe myocardial pathological changes and collagen volume fraction in the VMC group were significantly higher than in the control group at all three time points (P<0.05). Tranilast treatment significantly decreased the myocardial pathological changes and collagen volume fraction compared with the VMC group (P<0.05). The mRNA and protein expression of CTGF and Col I increased in the VMC group compared with the control group, and the increases were reduced with tranilast treatment (P<0.05). The number of MC was positively correlated to CTGF mRNA expression on the 7th day and 14th day (r=0.439, P=0.049) in the VMC group. There were positive correlations between the mRNA expression of Col I and CTGF on the 7th day and 14th day (r=0.646, P=0.007) and the 28th day (r=0.326, P=0.031).
conclusionsTranilast may inhibit the aggregation of MC and down-regulate the expression of CTGF, relieving myocardial fibrosis of mice with VMC.
Indexed as
Identifiers
27165596PMC7390369W2386691663What OpenQuestion holds
Registered trials
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