The Protective Effect Of Aspirin After Acute Ischemic Stroke

Object: Acute ischemic stroke is regarded as the second leading cause of death.As a primary antiplatelet agent,aspirin has been widely used for the prevetion of ischemic stroke.However,the specific mechanism in which aspirin improves ischemic stroke has poorly studied.Methods: An in vivo middle cerebral artery occlusion(MCAO)model was established in rats.The rats were divided into four groups: sham group;MCAO group;MCAO + saline group;Aspririn+MCAO group.Neurological Defects,cerebral Infarct Size and Reactive Oxygen Species(ROS)Production were determined.The protein levels of NOD2,JNK andNF-κB signaling were explored using western blot analysis.The levels of TNFα,IL-1β and IL-6 were studied with real time PCR.Results: After aspirin treatment,the neurological deficits,cerebral Infarct Size and ROS Production were significantly improved in comparison with saline group.Administration of aspirin significantly reduced the protein level of NOD2.Further study demonstrated the downstream signaling,NF-κB,and JNK activation,was obviously suppressed.Meanwhile,enhanced anti-apoptotic protein,Bcl-2,and decreased pro-apoptotic protein,Bax,can be detected.Consistent with the above data,the levels of TNFα,IL-1β and IL-6 were significantly suppressed in the aspirin group compared with saline group.Conclusions: To conclude,through suppressing NOD2-induced inflammatory responses and ROS production,aspirin treatment could alleviate the deterioration of cerebral function after acute ischemic stroke.