ArticleCurrent medical science2022
Blocking the Aryl Hydrocarbon Receptor Alleviates Myocardial Ischemia/Reperfusion Injury in Rats.
Article in Current medical science, 2022. 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.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Usp31 Promotes Cardiomyocyte Injury Under Ischemic Stress and Is Inhibited by Sodium Tanshinone IIA Sulfonate.Biomedicines · 2026Article
- Potential role of AhR in ischemia‑reperfusion injury and cancers: Focus on ferroptosis and lipid peroxidation signaling pathways (Review).International journal of molecular medicine · 2025Review
- Plasma aryl hydrocarbon receptor associated with epicardial adipose tissue in men: a cross-sectional study.Diabetology & metabolic syndrome · 2023Article
- Functions of the aryl hydrocarbon receptor (AHR) beyond the canonical AHR/ARNT signaling pathway.Biochemical pharmacology · 2023Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveRestoring the blood perfusion of ischemic heart tissues is the main treatment for myocardial ischemia. However, the accompanying myocardial ischemia reperfusion injury (IRI) would aggravate myocardial damage. Previous studies have confirmed that aryl hydrocarbon receptor (AhR) is closely correlated to kidney and intestinal IRI. The present study aimed to explore the relationship between AhR and myocardial IRI.
methodsAn oxygen glucose deprivation/reoxygenation (OGD/R) model of H9c2 cells and an ischemia/reperfusion (I/R) model of Sprague-Dawley rat myocardium were established. OGD/R cells and myocardial IRI rats were treated with different concentrations of the AhR antagonist CH-223191 or agonist 6-formylindolo[3,2-b] carbazole (FICZ). Under the conditions of normoxia and hypoxia/reoxygenation, the activity of cardiomyocytes, lactate dehydrogenase (LDH) and cell reactive oxygen species (ROS) were detected. In rats, myocardial pathological damage and markers of myocardial injury were detected.
resultsAccording to the results of the cell viability, LDH and ROS tests in vitro, both CH-223191 and FICZ showed no myocardial protection under OGD/R conditions. However, the histological staining and analysis of myocardial injury marker LDH in vitro revealed that CH-223191 could significantly reduce the myocardial IRI.
conclusionAhR exhibited a different effect on myocardial IRI in vitro and in vivo. In vivo, CH-223191 could significantly alleviate the myocardial IRI, suggesting that inhibition of AhR may play a role in myocardial protection, and AhR may serve as a potential treatment target for myocardial IRI.
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