ABSTRACT
Objective: Extracellular deposition of the beta-amyloid [A beta] peptide, which is the main finding in the pathophysiology of Alzheimer's disease [AD], leads to oxidative damage and apoptosis in neurons. Melissa officinalis [M. officinalis] is a medicinal plant from the Lamiaceae family that has neuroprotective activity. In the present study we have investigated the protective effect of the acidic fraction of M. officinalis on A beta-induced oxidative stress and apoptosis in cultured cerebellar granule neurons [CGN]. Additionally, we investigated a possible role of the nicotinic receptor
Materials and Methods: This study was an in vitro experimental study performed on mice cultured CGNs. CGNs were pre-incubated with different concentrations of the acidic fraction of M. officinalis for 24 hours, followed by incubation with A beta for an additional 48 hours. CGNs were also pre-incubated with the acidic fraction of M. officinalis and mecamylamin, followed by incubation with A beta. We used the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide [MTT] assay to measure cell viability. Acetylcholinesterase [AChE] activity, reactive oxygen species [ROS] production, lipidperoxidation, and caspase-3 activity were measured after incubation. Hochst/annexin V- fluorescein isothiocyanate [FITC]/propidium iodide [PI] staining was performed to detect apoptotic cells
Results: The acidic fraction could protect CGNs from A beta-induced cytotoxicity. Mecamylamine did not abolish the protective effect of the acidic fraction. AChE activity, ROS production, lipid peroxidation, and caspase-3 activity increased after A beta incubation. Pre-incubation with the acidic fraction of M. officinalis ameliorated these factors and decreased the number of apoptotic cells
Conclusion: Our results indicated that the protective effect of the acidic fraction of M. officinalis was not mediated through nicotinic receptors. This fraction could protect CGNs through antioxidant and anti-apoptotic activities