protective role of β-caryophyllene against lead acetate–induced cardiotoxicity in rats: effects on oxidative stress and antioxidant response

In this study, an experimental cardiotoxicity model was established in rats by administering lead acetate (pbac), and the effects of pbac on oxidative stress and tissue damage in the heart were investigated. furthermore, the potential protective role of β-caryophyllene (bcp), a natural plant-derived compound, against this toxic effect was evaluated. a total of 50 adult male sprague–dawley rats (220–290 g) were divided into five groups: control (physiological saline), bcp (400 mg/kg bcp, intragastric), pbac (30 mg/kg pbac, oral), bcp200+pbac (200 mg/kg bcp + 30 mg/kg pbac), and bcp400+pbac (400 mg/kg bcp + 30 mg/kg pbac). bcp, dissolved in olive oil, was administered intragastrically 30 minutes before pbac exposure. at the end of the experimental period, heart tissue samples were collected for biochemical and histopathological analyses. oxidative stress was assessed by measuring malondialdehyde (mda), superoxide dismutase (sod), glutathione (gsh), and glutathione peroxidase (gpx) levels. the pbac group exhibited a significant increase in mda levels and a marked decrease in sod, gsh, and gpx activities. in contrast, bcp-treated groups showed reduced mda levels and increased antioxidant enzyme activities. histopathological evaluation revealed pronounced myocardial degeneration, structural damage, and inflammatory cell infiltration in the pbac group, whereas bcp administration mitigated these changes and better preserved tissue integrity. these findings indicate that pbac induces severe cardiotoxicity at both biochemical and histological levels, and that bcp exerts a substantial protective effect by reducing oxidative stress and enhancing antioxidant defense systems.