Cardioprotective effect of Beta-caryophyllene on thioacetamide-induced heart damage in rats

Thioacetamide (TAA) is widely used in experimental toxicology to model liver diseases. However, recent findings indicate that TAA-induced liver injury can lead to structural and functional changes in the myocardium. This study evaluated the cardioprotective effects of beta-caryophyllene (BCP) against cardiac damage caused by TAA exposure in rats. In our research, 60 Sprague Dawley male rats were divided into 6 groups with 10 animals in each group. TAA (200 mg/kg) was administered intraperitoneally to rats for the first three days of the experiment, and BCP (100-200 mg/kg) was administered orally for 14 days. After the experiment, heart tissues were collected, and malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) levels were analyzed using manual biochemical methods, and PKR-like ER kinase (PERK), activating transcription factor (ATF-4), nuclear factor kappa B (NF-κB), and tumor necrosis factor-alpha (TNF-α) mRNA transcription levels were analyzed using RT-PCR. Furthermore, heart samples were examined histopathologically. Our findings showed that TAA exposure increased MDA levels in heart tissue and significantly decreased SOD and CAT activities. It also led to a significant increase in the expression levels of inflammatory markers (NF-κB and TNF-α) and ER stress biomarkers (PERK and ATF-4). BCP administration alleviated ER stress by suppressing PERK and ATF-4 expression. Furthermore, histopathological observations indicated that BCP treatment ameliorated TAA-induced cardiac tissue damage. BCP therapy relieved ER stress generated by oxidative damage and reduced the levels of inflammatory markers. Consequently, it was determined that BCP treatment may protect against cardiotoxicity by reducing TAA-induced oxidative stress, ER stress, and inflammation.