ArticleAmerican journal of translational research2022
Hydroxysafflor yellow A mitigates myocardial fibrosis induced by isoproterenol and angiotensin II.
Article in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Hydroxysafflor Yellow A improves diabetic nephropathy by inhibiting PI3K/AKT/mTOR pathway based on a multidimensional study.Frontiers in medicine · 2026Article
- Isoproterenol mechanisms in inducing myocardial fibrosis and its application as an experimental model for the evaluation of therapeutic potential of phytochemicals and pharmaceuticals.Animal models and experimental medicine · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsTo investigate the potential inhibitory effect of Hydroxysafflor yellow A (HSYA) on myocardial fibrosis induced by isoproterenol (ISO) and angiotensin II (Ang II) and the possible underlying mechanism.
methodsMice were injected subcutaneously with ISO and given HSYA by gavage in vivo. Masson's trichrome staining, immunohistochemical staining and immunofluorescence assays were conducted to evaluate the expression and localization of collagen and inflammatory cytokines, respectively. In vitro, cardiac fibroblasts (CFs) were treated with various doses of HSYA and induced with Ang II. Cell proliferation and migration were assessed using wound healing assay. Cell counting kit-8 was used to measure the cell viability. Collagen I, collagen III, phosphorylation of Smad2/3, Smad2/3, TGFβ1, interleukin (IL)-1β, IL-18, NLRP3 inflammasome-associated proteins were detected by Western blotting. Levels of reactive oxygen species (ROS) were evaluated using 2',7'-dichlorofluorescein diacetate assay.
resultsHSYA significantly inhibited ISO-induced myocardial fibrosis, NLRP3 inflammasome activation as well as IL-18 and IL-1β expressions in mice. HSYA significantly reduced the proliferation and migration of CFs, and suppressed the accumulation of collagen I and collagen III. TGFβ1 and P-Smad2/3 induced by Ang II was repressed by HSYA. HSYA downregulated IL-1β and IL-18, blocked NLRP3 activation, and reduced ROS in CFs.
conclusionHSYA may inhibit myocardial fibrosis by blocking NLRP3 pathway in CFs.
Indexed as
Identifiers
36628216PMC9827317What OpenQuestion holds
Registered trials
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