Key result
Britanin reduces infarct size and preserves cardiac function after MI by inhibiting JAK2/STAT3 signaling.
Why the study?
Current therapies offer limited myocardial protection in acute myocardial infarction, and the role of Britanin in AMI remains unclear.
Does Britanin alleviate myocardial damage and improve cardiac function in a rat model of acute myocardial infarction?
Does Britanin alleviate myocardial damage and improve cardiac function in a rat model of acute myocardial infarction?
Britanin demonstrates potential as a preclinical therapeutic agent for mitigating acute myocardial infarction injury by suppressing inflammation and pyroptosis.
Answers are grounded in this paper and cite their sources.
Britanin attenuates rat AMI injury; leaves open translation to human therapy.
Objectives: Acute myocardial infarction (AMI) is a life-threatening condition featuring coronary occlusion-induced myocardial ischemia-hypoxia, followed by tissue damage driven by calcium overload, inflammation, and pyroptosis. Current therapies offer limited myocardial protection. Britanin, a sesquiterpene lactone from Inula lineariifolia, has anti-inflammatory and antioxidant properties, while its role in AMI remains unclear. This study explored Britanin's therapeutic effects on rat AMI and underlying mechanisms, focusing on the JAK2/STAT3 signaling pathway. Materials and Methods: Network pharmacology, molecular docking, and ProTox3.0 toxicity prediction were used for target screening and safety evaluation. Rat AMI models were established by left anterior descending ligation and treated with Britanin (5/10 mg/kg). Echocardiography, serum biochemistry, histopathological staining, Western blotting, and qPCR were used to assess cardiac function, myocardial injury, fibrosis, and molecular changes. Results: 0.05), without liver or kidney toxicity. Conclusion: Britanin alleviates AMI-induced myocardial damage in rats by improving cardiac function, reducing injury and fibrosis, and inhibiting inflammation and pyroptosis through suppression of the JAK2/STAT3 pathway, positioning it as a potential AMI therapeutic agent.
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Zhang et al. (2026) studied Acute myocardial infarction (n=28). Britanin vs. Normal saline with co-solvents was evaluated on Myocardial infarct size and cardiac function (EF, LVFS) (p=<0.05). Britanin significantly improved cardiac function and reduced myocardial infarct size and fibrosis in rats with acute myocardial infarction by inhibiting the JAK2/STAT3 signaling pathway.
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