Abstract

Background and Objective: Ischemia is a stern decline or absolute obstruction in blood, flowing to various parts of the body. This pathophysiological episode causes cerebral mutilation, a protuberant feature of stroke, which is the 3rd leading cause of demise after cancer and heart attack globally. The principal objective of this work was to understand the sights of neuroprotection provided by M. Officinalis against OGD-R in rat’s brain cortex slices. Materials and Methods: Mitochondrial viability assays were performed via the colorimetric 3(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) method. After 2 h of oxygen and glucose deprivation (OGD) followed by 1 h of reperfusion, only viable slices showed the ability to trim down MTT into a purple "Formazan" product that was soluble in dimethyl sulfoxide (DMSO). Absorbance was measured at 570 and 630 nm and the net absorbance (A570-A630) was taken as an index of cell viability. Results: The results of the present investigation demonstrated that oxygen-glucose deprivation (OGD) followed by re-oxygenation led to cell damage/death via an amplifying ROS/free radicals production in rat’s brain cortex slices compared with control after 2 h OGD followed by 1h reperfusion. Melissa officinalis at a concentration of 40 μg mL–1 displayed potential role in neuro-protection against OGD, followed by re-oxygenation in mitochondrial viability assays in vitro. In addition, Melissa officinalis declined or slow down the production of free radicals in the supernatant and slices homogenate of cortex at the end of 2 h OGD followed by 1 h reperfusion. Furthermore, higher concentrations of Melissa officinalis slightly showed neurotoxicity for cortex slices which might be attributed to its pro-oxidant outcome. Conclusion: The results obtained during this study offer evidence for neuroprotective properties of M. officinalis against in vitro ischemia in rat’s cortex slices. Melissa officinalis could be considered as a therapeutic agent in the prevention of neuronal cell death in Ischemia induced by oxygen and glucose deprivation of cortex slices, strengthening further investigations to define the actual component for its use in human. Furthermore, in vivo ischemic models are now in progress to confirm and better characterize its neuroprotection.