Highlight: The potential of Pongamia pinnata as an inhibitor of apoptosis in ischemic stroke has never been evaluated before. Pongamia pinnata has potential to inhibit neuronal apoptosis via NMDAR and Caspase-3 in ischemic stroke. Karanjachromene has the best binding interaction to inhibit NMDAR.   ABSTRACT Introduction: One of the cardiovascular diseases with the highest mortality rate is stroke. Stroke is the second-leading cause of death worldwide. Each year, 12.2 million new cases of stroke occur, of which 7.6 million are ischemic strokes. In ischemic stroke, there are several pathways that cause neuronal apoptosis. The activity of NMDAR and caspase-3 is one of the pathways. Pongamia pinnata phytochemicals have a neuroprotective function against neurological disorders. However, its use as an inhibitor of apoptosis in ischemic stroke has never been evaluated before. Objective: This research was designed to evaluate the phytochemicals of Pongamia pinnata as inhibitors of neuronal apoptosis in ischemic stroke using an in silico study. Methods: This study used four main phytochemicals of Pongamia pinnata, namely Karanjin, Karanjachromene, Pongapin, and Pongachromene. The protein targets for neuronal apoptosis were NMDAR and caspase-3. The molecular docking processes were ligand preparation, protein preparation, grid box determination, molecular docking, and visualized molecular docking. Results: In silico results showed that at NMDAR target proteins, Karanjin, Karanjachromene, Pongapin, and Pongachromene have binding energies of -5.12, -5.83, -5.03, and -5.13 kcal/mol. At protein targets, Caspase-3, Karanjin, Karanjachromene, Pongapin, and Pongachromene have binding energies of -4.87, -4.98, -4.88, and -5.08 kcal/mol. Conclusion: The phytochemicals of Pongamia pinnata have the potential to inhibit neuronal apoptosis via NMDAR and caspase-3 in ischemic stroke. The binding of Karanjachromene to NMDAR demonstrated the compound's best interaction.

Background: Alzheimer's Disease (AD) is a neurodegenerative disorder with progressive impairment of behavioural and cognitive functions and the most common cause of dementia. The pathophysiology of AD is associated with low acetylcholine, accumulation of amyloid beta plaque, and neurofibrillary tangles in the brain. Cinnamomum zeylanicum is known to have many medicinal properties, especially neuroprotective effects. Objective: This research was designed to determine the neuroprotective potential of the phytochemicals C. zeylanicum using an in silico study. Methods: There are 5 phytochemicals compounds of C. zeylanicum used in this study. It's qualified for Lipinski’s rules of five and can cross blood brain barrier. The protein targets were AChE, BACE1, and GSK-3. Molecular docking and visualization were performed using Avogadro, AutoDock 4.2 PyMol and Biovia Discovery Studio 2019. Results: In silico results show that the main phytochemical compounds of C. zeylanicum Blume essential oil have great potency as an AD drug. The best interaction model of the compound was shown by trans-cinnamyl acetate and coumaric acid. Although the binding energy of the compounds is lower than AD drugs (donepezil, rivastigmine, galantamine), the binding energy is not much different from rivastigmine and galantamine. Conclusion: The phytochemical compounds of C. zeylanicum Blume essential oil have an effect as a neuroprotective agent for AD and should be investigated in future research.