Neuroprotective Effect of Quercetin during Cerebral Ischemic Injury Involves Regulation of Essential Elements, Transition Metals, Cu/Zn Ratio, and Antioxidant Activity.

Cerebral ischemia results in increased oxidative stress in the affected brain. Accumulating evidence suggests that quercetin possesses anti-oxidant and anti-inflammatory properties. The essential elements magnesium (Mg), zinc (Zn), selenium (Se), and transition metal iron (Fe), copper (Cu), and antioxidants superoxide dismutase (SOD) and catalase (CAT) are required for brain functions. This study investigates whether the neuroprotective effects of quercetin on the ipsilateral brain cortex involve altered levels of essential trace metals, the Cu/Zn ratio, and antioxidant activity. Rats were intraperitoneally administered quercetin (20 mg/kg) once daily for 10 days before ischemic surgery. Cerebral ischemia was induced by ligation of the right middle cerebral artery and the right common carotid artery for 1 h. The ipsilateral brain cortex was homogenized and the supernatant was collected for biochemical analysis. Results show that rats pretreated with quercetin before ischemia significantly increased Mg, Zn, Se, SOD, and CAT levels, while the malondialdehyde, Fe, Cu, and the Cu/Zn ratio clearly decreased as compared to the untreated ligation subject. Taken together, our findings suggest that the mechanisms underlying the neuroprotective effects of quercetin during cerebral ischemic injury involve the modulation of essential elements, transition metals, Cu/Zn ratio, and antioxidant activity.

Resveratrol Mitigates Cerebral Ischemic Injury by Altering Levels of Trace Elements, Toxic Metal, Lipid Peroxidation, and Antioxidant Activity.

Cerebral ischemia causes increased oxidative stress due to the overproduction of reactive oxygen species. The polyphenol compound resveratrol exerts neuroprotective effects through its antioxidant and anti-inflammatory abilities. The trace elements magnesium (Mg), zinc (Zn), and selenium (Se) also exert antioxidant properties. This study mainly investigates whether the neuroprotective effect of resveratrol during cerebral ischemia is related to its modulation of the concentrations of trace element and toxic metal lead (Pb). Experimental rats were administered resveratrol (20 mg/kg) once daily for 10 consecutive days. Cerebral ischemia was surgically induced via ligation of the right middle cerebral artery and right common carotid artery for 1 h. Brain cortex tissues were homogenized, and the supernatants were harvested for biochemical analysis. Experimental results showed that rats pretreated with resveratrol before cerebral ischemia had significantly higher trace element concentrations of Mg, Zn, and Se and higher antioxidant activity (superoxide dismutase and catalase) in the brain cortex as compared to untreated cerebral ischemia rats. Conversely, resveratrol pretreatment markedly attenuated lipid peroxidation and concentrations of the toxic metal Pb as compared to untreated cerebral ischemic rats. Altogether, the findings of this study highlight that the mechanism underlying the neuroprotective effect of resveratrol involves modulation of the brain levels of trace elements, toxic metal lead, lipid peroxidation, and antioxidant activity.