Iranian journal of basic medical sciences · 2026
Britanin alleviates myocardial damage in rats with acute myocardial infarction by inhibiting the JAK2/STAT3 signaling pathway.
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Zhang Yiqing, Li Xian, Jiang Hezi, Zhang Guoxing, Zhou Yafeng
Аннотация
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: 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.
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.