Iranian Journal of Basic Medical Sciences

Iranian Journal of Basic Medical Sciences

Britanin alleviates myocardial damage in rats with acute myocardial infarction by inhibiting the JAK2/STAT3 signaling pathway

Articles in Press

Document Type : Original Article

Authors
Yiqing Zhang 1, 2
Xian Li 1
Hezi Jiang 1
Guo-Xing Zhang 3
Yafeng Zhou 1
1 Department of Cardiology, The Fourth Affiliated Hospital of Soochow University, Medical Center of Soochow University, Suzhou Dushu Lake Hospital, Suzhou City, Jiangsu Province, P. R. China
2 Department of Cardiology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou City, Jiangsu Province, P. R. China
3 Department of Physiology and Neurosciences, Medical College of Soochow University, Suzhou City, Jiangsu Province, P. R. China
10.22038/ijbms.2026.94760.20444
Abstract
Objective(s): 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: Pharmacology identified 30 overlapping targets, including JAK2, and highlighted JAK2/STAT3 as a key pathway. Britanin bound JAK2 strongly (binding energy <-8.2 kcal/mol); its LD50 was 150 mg/kg, indicating safety. Britanin improved cardiac function indices, alleviated myocardial fibrosis, reduced serum injury markers, and down-regulated components of the JAK2/STAT3 pathway, the NLRP3 (NOD-like receptor pyrin domain-containing 3) inflammasome, and pyroptosis markers (all P<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.
Keywords
Acute myocardial infarction
Britanin
JAK2/STAT3 signaling- pathway
NLRP3 inflammasome
Pyroptosis
Subjects
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Iranian Journal of Basic Medical Sciences

Articles in Press, Accepted Manuscript
Available Online from 22 September 2026