New prospects for drug treatment of chronic cerebral ischemia from the standpoint of neuroinflammation

Abstract

The high prevalence of stroke worldwide requires a revision of the modern doctrine of the management of patients with cerebrovascular disease. It is obvious that only aggressive modification of risk factors for vascular pathology does not guarantee the prevention of acute cerebrovascular accident, which is an intermediate or final stage of cerebrovascular disease. In this regard, the use of neuroprotectors, including vinpocetine, can increase the tolerance of brain tissue to hypoxia. Vinpocetine, a derivative of the alkaloid vincamine, inhibiting phosphodiesterase and voltage-dependent Na+- channels is widely used in many countries for the treatment of cerebrovascular diseases, including chronic cerebral ischemia. Recent studies have identified a number of new therapeutic effects of vinpocetine, including stimulation of neuroplasticity via brain-derived neurotrophic factor and inhibition of neuroinflammation. The latter mechanism is mediated by the effect on NF-kB that suppresses the expression of NF-kBdependent pro-inflammatory molecules and prevents the formation of NLRP3 inflammasome. New data allow to reconsider the place of vinpocetine in the prevention and treatment of cerebrovascular disorders, and to recommend its use in a wide range of patients with chronic cerebral ischemia.