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Cerebral ischemia induces oxidative brain injury via increased oxidative stress. Epigallocatechin gallate (EGCG) exerts anti-oxidant, anti-inflammatory, and metal chelation effects through its active polyphenol constituent. This study investigates whether EGCG protection against cerebral ischemia-induced brain cortex injury occurs through modulating lipid peroxidation, antioxidant activity, the essential elements of selenium (Se), zinc (Zn), magnesium (Mg), copper (Cu), iron (Fe), and copper (Cu), Zn/Cu ratio, and the hazardous metal lead (Pb). Experimentally, assessment of the ligation group was performed by occlusion of the right common carotid artery and the right middle cerebral artery for 1 h. The prevention group was intraperitoneally injected with EGCG (50 mg/kg) once daily for 10 days before cerebral ischemia. The brain cortex tissues were homogenized and the supernatants were harvested for biochemical analysis. Results indicated that cerebral ischemia markedly decreased SOD, CAT, Mg, Zn, Se, and Zn/Cu ratio and increased malondialdehyde (MDA), Fe, Cu, and Pb in the ischemic brain cortex. Notably, pretreating rats with EGCG before ischemic injury significantly reversed these biochemical results. Our findings suggest that the neuroprotection of EGCG in the ischemic brain cortex during cerebral ischemia involves attenuating oxidative injury. Notably, this neuroprotective mechanism is associated with regulating lipid peroxidation, antioxidant activity, essential elements, Zn/Cu ratio, and hazardous metal Pb.

Cerebral ischemia is related to increased oxidative stress. Resveratrol displays anti-oxidant and anti-inflammatory properties. The transition elements iron (Fe) and copper (Cu) are indispensable for the brain but overload is deleterious to brain function. Aluminum (Al) and arsenic (As) are toxic metals that seriously threaten brain health. This study was conducted to elucidate the correlation of the neuroprotective mechanism of resveratrol to protect cerebral ischemic damage with modulation of the levels of lipid peroxidation, anti-oxidants, transition elements, and toxic metals. Experimentally, 20 mg/kg of resveratrol was given once daily for 10 days. The cerebral ischemic operation was performed via occlusion of the right common carotid artery together with the right middle cerebral artery for 60 min followed by homogenization of the brain cortex and collection of supernatants for biochemical analysis. In the ligation group, levels of malondialdehyde, Fe, Cu, Al, and As increased but those of the anti-oxidants superoxide dismutase and catalase decreased. Pretreating rats with resveratrol before ischemia significantly reversed these effects. Our findings highlight the association of overload of Fe, Cu, As, and Al with the pathophysiology of cerebral ischemia. In conclusion, resveratrol protects against cerebral ischemic injury via restraining lipid peroxidation, transition elements, and toxic metals, but increasing anti-oxidant activity.