Cardioprotective effects of Bassia indica via NF-κB and BCL-2/BAX modulation in isoproterenol-induced myocardial injury.

Background: Myocardial infarction (MI) is a fatal coronary heart disease that develops due to prolonged hypoxia. During MI progression, uncontrolled inflammation and apoptosis mediated by NF-κB and BAX/BCL-2 signaling pathways potentiate cardiac injury. Phenolic and flavonoid-rich medicinal plants have shown efficacy in suppressing the inflammatory pathways, thus reducing the adverse cardiac remodeling. In this study, we evaluated the cardioprotective and anti-inflammatory potential of Bassia indica (Wight) A.J. Scott, a plant traditionally used for treating cardiac disorders. Methods: B. indica extract (BiE) was prepared and characterized by UHPLC-MS/MS. Its anti-inflammatory activity was determined by in vitro inhibition of COX-2 and 5-LOX enzymes, followed by in vivo suppression of acute inflammation induced by carrageenan, histamine, and serotonin. The role of the anti-inflammatory activity in the amelioration of myocardial injury was assessed by isoproterenol (ISO)-induced MI, and qPCR studies were performed to explore underlying mechanisms. Results: UHPLC/MS/MS analysis of BiE tentatively identified several plant metabolites, including kaempferol 3-glucoside-7-sophoroside, kaempferol 3-rutinoside-7-sophoroside, and kaempferol 3-(2G-glucosylrutinoside), and phenolic derivatives. It inhibited COX-2 (IC50 = 0.6 μg/mL) and 5-LOX (IC50 = 8.3 μg/mL) enzymes. BiE-treated animals exhibited reduced inflammation in response to carrageenan, histamine, and serotonin. Pretreatment with BiE significantly reduced the infarct size; preserved cardiac tissue architecture; lowered cardiac biomarkers (cTnI, CK-MB, LDH, and AST); downregulated NF-κB, COX-2, TNF-α, and IL-1β; and upregulated IL-10 and BCL-2. Conclusion: These findings suggest that BiE has cardioprotective effects that are mediated by the suppression of inflammation and apoptosis.