ArticleBMC cardiovascular disorders2025
Effects of nicorandil on inflammatory response, oxidative stress and myocardial fibrosis after myocardial infarction.
Article in BMC cardiovascular disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
introductionNumerous studies have established the potential of nicorandil in alleviating myocardial fibrosis subsequent to myocardial infarction. Nevertheless, the precise mechanism underlying this effect remains incompletely elucidated. This study aims to investigate whether nicorandil can mitigate myocardial inflammation and oxidative stress during post-infarction remodeling in mice through animal experiments, thereby shedding light on its mechanism for ameliorating myocardial fibrosis after myocardial infarction by inhibiting inflammation and oxidative stress.
methodsThe male C57BL/6J mice were randomly allocated into the following groups: Sham group, MI group, Nic group and Nic + Glib group. The left anterior descending coronary artery (LAD) was ligated to induce myocardial infarction. The intervention lasted for 4 weeks after modeling in each group. Cardiac function was evaluated by echocardiography and cardiac mass index. Serum hs-CRP was quantified using ELISA. The oxidative stress level of myocardial tissue was determined using an oxidative stress detection box. HE staining and Masson staining were employed to evaluate the inflammatory response and fibrosis in myocardial tissue. Immunohistochemical staining was utilized to detect the inflammatory response and fibrosis markers in local myocardial tissue: IL-1β,TNF-α,IL-6,α-SMA and CollagenⅠ.
resultsNicorandil can improve left ventricular fractional shortening (LVFS%), left ventricular ejection fraction (LVEF%), and heart mass index after myocardial infarction, and reduce serum hs-CRP and the expression of IL-1β, TNF-α, IL-6, α-SMA, and collagenⅠ in myocardial tissue. In addition, it can increase SOD and GSH-Px levels and reduce MDA content in myocardial tissue. In addition, HE and Masson staining showed that nicorandil could inhibit myocardial and perivascular fibrosis to a certain extent, and reduce the level of local inflammatory response. These beneficial effects of nicorandil were inhibited to some extent by glibenclamide.
conclusionNicorandil attenuates myocardial inflammation, oxidative stress and myocardial fibrosis levels by activating ATP-sensitive potassium channels (K-ATP), thereby improving post-MI cardiac remodeling and preserving cardiac function.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.