Myrrhone exert cardioprotective effect against isoproterenol-induced myocardial injury in rats via alteration of NF-κB and Bax/Bcl-2/caspase-3 signaling.

PURPOSE: To examine the cardioprotective effects of myrrhone against isoproterenol (ISO)-induced myocardial injury in rats.

METHODS

Myocardial injury was induced in the rats through subcutaneous administration of ISO (85 mg/kg). The body weight, heart weight, electrocardiogram (ECG), cardiac, antioxidant, electrolyte, membrane-bound enzymes, antioxidant, cytokines, and inflammatory parameters were estimated. The mRNA expression of inflammatory parameters was estimated in the cardiac tissue.

RESULTS

Myrrhone treatment significantly (p < 0.001) altered ECG parameters, body weight, heart weight, and heart weight/body weight ratio. Myrrhone significantly (p < 0.001) improved the level of 5-hydroxytryptamine (5-HT) and suppressed the level of cardiac parameters like creatine kinase-MB, creatine kinase, lactate dehydrogenase, cardiac troponin I, and cardiac troponin T. It also suppressed the level of hepatic parameters such as aspartate aminotransferase, and alanine transaminase; altered the electrolyte, membrane-bound enzymes, and antioxidant parameters. Myrrhone treatment significantly (p < 0.001) altered the level of cytokines such as tumor necrosis factor-α (TNF-α), interleukin (IL)-10, IL-1β, IL-17, and IL-6; inflammatory parameters like cyclooxygenase-2, prostaglandin, inducible nitric oxide synthetase, nuclear factor kappa-light-chain enhancer of activated B cells; matrix metalloproteinases such as 2, and 9; apoptosis parameters viz., Bcl-2-associated X protein (Bax), B-cell lymphoma 2 protein (Bcl-2), and caspase-3 parameters. Myrrhone treatment significantly (p < 0.001) altered the mRNA expression IL-6, IL-1β, IL-10, TNF-α, Bcl-2, caspase-3, Bax, and caspase-9.

CONCLUSION

Myrrhone exhibited the cardioprotective effect against ISO-induced myocardial injury in rats via alteration of kappa-light-chain enhancer of activated B cells (NF-κB) and Bax/Bcl-2/caspase-3 signaling.