Ischemic stroke is the disruption of blood flow to a part of the brain. Without oxygen, some neurons die by apoptosis and other neurons experiencing energy failure are not able to complete apoptosis, therefore end up in necrosis and give rise to inflammatory conditions. However, during the first few hours after the first signs of symptoms, the neurons present in an region called penumbra, which commence to die by apoptosis, could be saved by either allowing the blood flow to restart or using antiapoptotic drugs, therefore promoting neuroprotection. In this regard, our group developed a new antiapoptotic and anti-inflammatory drug derived from tobacco leaves named 4R. Strong in vitro and in vivo evidences suggests two possible mechanisms of neuroprotection by 4R after brain ischemia, one is due to Akt activation, a well known antiapoptotic and anti-inflammatory protein and the second one is by decrease of cytokine release. We are currently evaluating these possible mechanism of action of 4R. In the same umbrella of neuroprotection our group is also verifying the action of cholinergic system and renin-angiotensin system using transient middle cerebral artery occlusion as in vivo model of stroke in rats.