Lipid peroxidation reduction and hippocampal and cortical neurons protection against ischemic damage in animal model using .

This study was aimed to determine the neuroprotective influence of in terms of restoring normal state of the rat's hippocampus and cortex after oxidative insult caused by ischemia and reperfusion. Cell viability and membrane integrity were assessed using MTT and lactate dehydrogenase (LDH) assay, respectively. Ischemic insult was introduced in the rat brain's hippocampal and cortical slivers by exposing oxygen and glucose deficiency (OGD) for 2 h, followed by 1 h of re-perfusion. Cellular oxidative stress levels were quantified by incorporating 2',7'-dichlorofluorescein diacetate fluorescent probes. Additionally, the lipid peroxidation was assessed using TBARS assay. Findings revealed significant neuroprotection against OGD-induced mitochondrial impairment at 40 µg/mL of in rat's hippocampal and cortical slices. The LDH levels were decreased significantly ( < 0.001) during pre-incubation and reoxygenation periods using varied concentrations of extract. Cellular oxidative stress levels results showed significant ( < 0.001) reduction in dichlorofluorescein fluorescence in slices homogenate of hippocampus and cortex using extract. The lipid peroxidation assay results showed decreased ( < 0.01) levels of malondialdehyde in liver tissues of treated rats treated (200 mg/kg body weight) when compared to the ischemic animal. In summary, findings clearly indicated the neuroprotective effects of extract against ischemia in brain hippocampal and cortex slivers. could undoubtedly be utilized as a healing agent in preventing neuronal cells' loss during is chemic-reperfusion process.