ArticleJournal of cardiovascular translational research2026
Baicalin Attenuates Oxidative Stress and Apoptosis in Myocardial Ischemia/reperfusion Injury via Suppression of STING/NLRP3 Pathway.
Article in Journal of cardiovascular translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Ischemic heart disease, as one of the major causes of morbidity worldwide, there is no effective therapy for preventing myocardial ischemia-reperfusion injury (MIRI). Baicalin, a flavonoid glycoside extracted from the Scutellaria baicalensis Georgi, yet its effects in MIRI remain unclear. In the study, pretreatment with Baicalin (100 mg/kg, i.p.) markedly alleviated I/R-induced cardiac dysfunction, as shown by reduced serum lactate dehydrogenase (LDH), creatine kinase (CK), and myocardial infarction. Baicalin also improved cardiomyocyte survival by increasing Bcl-2 and decreasing Bax and caspase-3/9 levels. In addition, Baicalin suppressed oxidative stress by reducing malondialdehyde (MDA) while elevating glutathione (GSH) and superoxide dismutase (SOD) levels. Moreover, Baicalin inhibited the STING, NLRP3, cleaved caspase-1, IL-18, and IL-1β expression in vivo and in vitro. Crucially, amidobenzimidazole (ABZI), a STING agonist, reversed the cardioprotective effects of Baicalin. Collectively, these findings demonstrated that Baicalin exerted cardioprotective effects by attenuating apoptosis and oxidative stress through suppression of STING/NLRP3 activation.
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