Therapeutic effects of Biochanin A against CCl4-induced cardiac toxicity: enhancing antioxidant defenses and modulating inflammatory responses

• Biochanin A reduces CCl4-induced cardiac injury in rats. • Biochanin A significantly improves lipid profiles disrupted by CCl4. • Biochanin A boosts antioxidant enzymes (SOD, CAT, GPx) and reduces oxidative stress. • Biochanin A decreases inflammatory markers (Hs-CRP, IL-6, TNF-α) in cardiac tissue. • Biochanin A shows therapeutic promise for cardiovascular disease prevention. Cardiovascular damage caused by environmental toxins, such as carbon tetrachloride (CCl 4 ), is closely associated with oxidative stress and inflammatory injury. Biochanin A, an isoflavone isolated from Trifolium pratense L., has been demonstrated to be a prospective candidate in rational phytotherapy based on its anti-oxidative and anti-inflammatory activity. The present study was conducted to explore the therapeutic potential of Biochanin A against CCl₄-induced cardiac toxicity in rats, with an emphasis on its pharmacological mode of action via regulating oxidative stress & pro-inflammatory cytokines. Experimental animal study. Twenty-four Wistar albino rats were divided into four groups, including control, CCl 4 , and CCl 4 + Biochanin A, at 50 mg/kg and 100 mg/kg doses. Assessment of lipid profile, oxidative stress markers (MDA, SOD, CAT, GPx), cardiac function enzymes (lactate dehydrogenase, creatine kinase), and inflammatory markers (Hs-CRP, IL-6, TNF-α) was done. To our knowledge, this study is the first to show that Biochanin A has a dose-dependent therapeutic effect on CCl₄-induced cardiac toxicity in rats. Previous studies mainly investigated the effects of Biochanin A in models of hepatic, renal, or metabolic damage. Whereas the present investigation establishes its direct cardioprotective potential in an acute oxidative and inflammatory stress setting. Treatment with Biochanin A robustly antagonized the effects evoked by CCl 4 , particularly in lipid metabolism. Specifically, animals treated with Biochanin A had significantly decreased triglycerides, LDL, and VLDL levels; HDL levels that benefit cardiovascular health were brought closer to normal ranges. In addition, treatment with Biochanin A decreased malondialdehyde levels, suggesting diminished lipid peroxidation. Another beneficial effect was an increased activity of enzymes such as SOD, CAT, and GPx, which indicated that the antioxidant defense system was improved. Furthermore, reducing Hs-CRP, IL-6, and TNF-α levels significantly improves the inflammatory profile, offsetting systemic inflammatory and cardiac stress. Biochanin A protects against CCl 4 -mediated cardiac injury by modulating lipid metabolism, increasing antioxidant status, and suppressing inflammation, underscoring its potential as a therapeutic for CVDs.