ArticleActa pharmacologica Sinica2022
Glibenclamide alleviates β adrenergic receptor activation-induced cardiac inflammation.
Article in Acta pharmacologica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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16 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- The Effects of Combined Antihypertensive and Antidiabetic Therapies on Cardiovascular Outcomes: A Systematic Review and Meta-Analysis.Diabetes, obesity & metabolism · 2026Pooled it
- Glibenclamide attenuates osteoarthritis by suppressing NLRP3 inflammasome activation in synovial macrophages through the MAPK pathway.Journal of translational medicine · 2026Article
- Research advances on NLRP3 inflammasomes in organ transplantation.Frontiers in immunology · 2026Review
- Identification and experimental validation of mitochondrial and endoplasmic reticulum stress related gene in diabetic nephropathy.Scientific reports · 2025Article
- P2X7 receptor is essential for ST36-attenuated cardiac fibrosis upon beta-adrenergic insult.Purinergic signalling · 2025Article
- Miglustat ameliorates isoproterenol-induced cardiac fibrosis via targeting UGCG.Molecular medicine (Cambridge, Mass.) · 2025Article
- Ibogaine Induces Cardiotoxic Necrosis in Rats-The Role of Redox Processes.International journal of molecular sciences · 2024Article
- Therapies for Cirrhotic Cardiomyopathy: Current Perspectives and Future Possibilities.International journal of molecular sciences · 2024Review
- Isoproterenol induces MD2 activation by β-AR-cAMP-PKA-ROS signalling axis in cardiomyocytes and macrophages drives inflammatory heart failure.Acta pharmacologica Sinica · 2024Article
- Effects of Phenylacetylglutamine on the Susceptibility of Atrial Fibrillation in Overpressure-Induced HF Mice.Molecular and cellular biology · 2024Article
- Protective Effects of 2-Methoxyestradiol on Acute Isoproterenol-Induced Cardiac Injury in Rats.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023Article
- Zanubrutinib Ameliorates Cardiac Fibrosis and Inflammation Induced by Chronic Sympathetic Activation.Molecules (Basel, Switzerland) · 2023Article
- Noise exposure and its relationship with postinfarction cardiac remodeling: implications for NLRP3 inflammasome activation.Bioengineered · 2022Article
- The Mechanism and Regulation of the NLRP3 Inflammasome during Fibrosis.Biomolecules · 2022Review
- The Role of NLRP3 Inflammasome in Diabetic Cardiomyopathy and Its Therapeutic Implications.Oxidative medicine and cellular longevity · 2022Review
- Resveratrol Targets AKT1 to Inhibit Inflammasome Activation in Cardiomyocytes Under Acute Sympathetic Stress.Frontiers in pharmacology · 2022Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
β-Adrenergic receptor (β-AR) overactivation is a major pathological factor associated with cardiac diseases and mediates cardiac inflammatory injury. Glibenclamide has shown anti-inflammatory effects in previous research. However, it is unclear whether and how glibenclamide can alleviate cardiac inflammatory injury induced by β-AR overactivation. In the present study, male C57BL/6J mice were treated with or without the β-AR agonist isoprenaline (ISO) with or without glibenclamide pretreatment. The results indicated that glibenclamide alleviated ISO-induced macrophage infiltration in the heart, as determined by Mac-3 staining. Consistent with this finding, glibenclamide also inhibited ISO-induced chemokines and proinflammatory cytokines expression in the heart. Moreover, glibenclamide inhibited ISO-induced cardiac fibrosis and dysfunction in mice. To reveal the protective mechanism of glibenclamide, the NLRP3 inflammasome was further analysed. ISO activated the NLRP3 inflammasome in both cardiomyocytes and mouse hearts, but this effect was alleviated by glibenclamide pretreatment. Furthermore, in cardiomyocytes, ISO increased the efflux of potassium and the generation of ROS, which are recognized as activators of the NLRP3 inflammasome. The ISO-induced increases in these processes were inhibited by glibenclamide pretreatment. Moreover, glibenclamide inhibited the cAMP/PKA signalling pathway, which is downstream of β-AR, by increasing phosphodiesterase activity in mouse hearts and cardiomyocytes. In conclusion, glibenclamide alleviates β-AR overactivation-induced cardiac inflammation by inhibiting the NLRP3 inflammasome. The underlying mechanism involves glibenclamide-mediated suppression of potassium efflux and ROS generation by inhibiting the cAMP/PKA pathway.
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