Hesperidin alleviates streptozotocin-induced cardiac damage in rats through modulation oxidative stress, inflammation and apoptosis

This study investigated the potential cardioprotective effects of hesperidin (HES) against cardiac damage induced by streptozotocin (STZ)-mediated diabetes in rats. Diabetes was induced by a single intraperitoneal injection of STZ (45 mg/kg) and HES (100 mg/kg/day) were administered intragastrically to treatment groups for 14 days. Cardiac tissue samples were analyzed using the ELISA method for Total Antioxidant Status (TAS) Total Oxidant Status (TOS) malondialdehyde (MDA) and glutathione (GSH) levels, while inflammatory (TNF-α) and apoptotic (Caspase-3) markers were assessed immunohistochemically. STZ administration resulted in significantly increased TNF-α expression, TOS and MDA levels, and reduced TAS and GSH levels, accompanied by severe myocardial degeneration, necrosis, and vascular congestion. HES treatment markedly improved antioxidant status, decreased oxidative and inflammatory markers, and reduced apoptosis. Histopathological evaluations demonstrated substantial preservation of cardiac morphology in the STZ+HES group. Overall, these findings suggest that HES has a protective effect against diabetes-induced cardiac injury, likely through the modulation of oxidative stress, inflammation, and apoptosis.