ArticleFrontiers in pharmacology2024
Suppression of NLRP3 inflammasome orchestrates the protective efficacy of tiron against isoprenaline-induced myocardial injury.
Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Nano gold-loaded Nannochloropsis oculata attenuates fluoride-induced neural and hepatorenal toxicity by modulating the Nrf2/NF-κB axis and aquaporins.Biology direct · 2026Article
- Amelioration of contusion-induced muscle injury via regulation of the NLRP3 inflammasome.International journal of medical sciences · 2026Article
- Modulation of Cardiac Gene Expression by anti-HMGB1 in a Model of Experimental Myocardial Infarction.Physiological research · 2025Article
- Magnesium-assisted hydrogen improves isoproterenol-induced heart failure.Medical gas research · 2025Article
- Renoprotective impact of tiron against diclofenac-induced nephrotoxicity: targeting TLR4/NF-κB/NLRP3/Caspase-1/IL1-β pathway.BMC pharmacology & toxicology · 2025Article
- Liraglutide Treatment Restores Cardiac Function After Isoprenaline-Induced Myocardial Injury and Prevents Heart Failure in Rats.Life (Basel, Switzerland) · 2025Article
- Genetic Factors Associated With Myocardial Infarction in Saudi Arabia.Journal of the Saudi Heart Association · 2025Review
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16 authors.
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Abstract
The major contribution of myocardial damage to global mortalities raises debate regarding the exploration of new therapeutic strategies for its treatment. Therefore, our study investigated the counteracting effect of tiron against isoprenaline (ISO)-mediated cardiac infarction in mice. Tiron was administered to mice for 7 days prior to two consecutive injections of ISO on days 8 and 9 of the treatment protocol. Tiron significantly reduced the levels of CK-MB, LDH, and AST in serum samples of ISO-challenged mice. A considerable increase in the cardiac antioxidant response was observed in tiron-treated mice, as indicated by depletion of MDA and enhancement of antioxidant activities. Furthermore, tiron induced a marked decrease in NLRP3, ASC, and caspase-1 levels accompanied by weak immune reactions of IL-1β, NF-κB, TLR4, and iNOS in the infarct cardiac tissues. Histopathological screening validated these variations observed in the cardiac specimens. Thus, tiron clearly mitigated the oxidative and inflammatory stress by repressing the NLRP3 inflammasome and the TLR4/NF-κB/iNOS signaling cascade.
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Registered trials
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