Vinpocetine (VPN) is a synthetic ethyl-ester derivative of the alkaloid apovincamine from Vinca minor leaves. VPN is a selective inhibitor of phosphodiesterase type 1 (PDE1) that has potential neurological effects through inhibition of voltage-gated sodium channel and reduction of neuronal calcium influx. VPN has noteworthy antioxidant, anti-inflammatory, and anti-apoptotic effects with inhibitory effect on glial and astrocyte cells during and following ischemic stroke (IS). VPN is effective as adjuvant therapy in the management of epilepsy; it reduces seizure frequency by 50% in a dose of 2 mg/kg/day. VPN improves psychomotor performances through modulation of brain monoamine pathway mainly on dopamine and serotonin, which play an integral role in attenuation of depressive symptoms. VPN recover cognitive functions and spatial memory through inhibition of hippocampal and cortical PDE1 with augmentation of cyclic adenosin monophosphate and cyclic guanosin monophosphate ratio, enhancement of cholinergic neurotransmission, and inhibition of neuronal inflammatory mediators. Therefore, VPN is an effective agent in the management of IS and plays an integral role in the prevention and attenuation of poststroke epilepsy, depression, and cognitive deficit through direct cAMP/cGMP-dependent pathway or indirectly through anti-inflammatory and antioxidant effects.

No abstract

Background: Acute ischemic strokes (AIS) are a common cause of morbidity, mortality, and disability. The serum biomarker S100β correlates with poor neurological outcomes in the setting of AIS. This study describes the impact of statin treatment on S100β levels following AIS. Methods: This was a prospective case–control study of AIS patients compared to healthy controls. Patients were stratified into three groups: (1) AIS patients on statin therapy, (2) AIS patients not on statin therapy, and (3) healthy controls. Demographics, clinical parameters, stroke risk scores (SRS), and S100β levels were recorded for all patients. Results: Blood pressure, lipids, and SRS scores were higher in stroke versus control patients (all P < 0.05), and lower in Group I versus II (all P < 0.05). S100β levels were higher in stroke versus nonstroke patients ( P = 0.001), and lower in Group I versus II ( P = 0.001). Furthermore, patients on atorvastatin showed greater S100β reductions than those on rosuvastatin therapy ( P = 0.01). Conclusion: In acute stroke patients, statins therapy correlated with reductions in the neuronal injury biomarker S100β, with greater reductions observed for atorvastatin than rosuvastatin therapy.

No abstract

No abstract