Redox and apoptosis modulation by telmisartan, ertugliflozin, and omaveloxolone in a rat model of global cerebral ischemia/reperfusion injury

Ischemic stroke, accounting for 87% of all stroke cases, is a major global health issue associated with global cerebral ischemia. This study aimed to evaluate the neuroprotective effects of telmisartan, ertugliflozin, and omaveloxolone on cerebral ischemia–reperfusion injury. Forty-two rats were randomly assigned to seven groups. Their brain tissues were collected for infarct size assessment using triphenyltetrazolium chloride (TTC) staining and for ELISA analysis of oxidative and apoptotic markers, including superoxide dismutase (SOD), catalase (CAT), caspase-3, BCL2-associated protein X (BAX), B cell lymphoma-2 (BCL2), and the BCL2/BAX ratio. Pretreatment significantly reduced infarct area ( P < 0.05), as determined by TTC staining. All three treatments significantly increased antioxidant enzyme levels, including SOD and CAT ( P < 0.05). The treated groups showed a substantial decrease in caspase-3 levels, increased BCL2 expression, and a higher BCL2/BAX ratio ( P < 0.05). Telmisartan, ertugliflozin, and omaveloxolone each produced neuroprotective benefits, preserving brain tissue largely through their antioxidant and anti-apoptotic actions.