Pharmacological and non-pharmacological methods of protection of brain tissues from ischemia/reperfusion injury

 

Cerebrovascular accident is one of the leading causes of morbidity and mortality worldwide. A treatment strategy for ischemic stroke, that aims to prevent, suppress or inhibit biochemical and molecular processes leading to irreversible ischemic neuronal damage, is called neuroprotection.

Priority data on the effects of different protocols of ischemic postconditioning on the neuronal viability of hippocampus and cerebral cortex, as well as on the cytoplasmic activity of the key enzymes of energetic metabolism (lactate dehydrogenase, succinate dehydrogenase) were obtained in the study of endogenous neuroprotective mechanisms. An infarct size-limiting effect of ischemic postconditioning was investigated, and an analysis of the relationship between the anatomical variation of the middle cerebral artery cortical branch and infarct size was performed on a model of focal ischemia/reperfusion injury in the rat brain. It has been established that the amino acid L-theanine found in green tea causes a reduction of cerebral infarct size when administered 3 and 12 hours after reperfusion, but not 24 hours after reperfusion. Repeated administration of L-theanine in the striatum has prevented the brain injury caused by administration of glutamate receptor agonists. The study of neuroprotective effect of natural products, particularly a natural polyphenol, curcumin, is continuing.

Studies on the effectiveness of substances and drugs with potential neuroprotective activity are carried out in accordance with international recommendations STAIR 1 (1999), STAIR 2 (2009), and RIGOR (2012), i. e., adequate physiological monitoring, randomization, blinding, description of inclusion/exclusion criteria as well as histological and functional evaluation criteria of damage in acute (1-3 days) and late (7-30 days) periods.