Effect of Thrombin on Cultured Rat Astrocytes Exposed to Oxygen-Glucose Deprivation

Cerebral ischemia is a complex of damaging factors, which include oxygen and glucose deprivation, as well as the possibility of repeated lesions during the period of tissue reperfusion. Thrombin, a key serine protease of hemostasis, can be found in the brain parenchyma in ischemic and hemorrhagic strokes, where it enters directly from the bloodstream through the damaged blood-brain barrier (BBB). In this work, the effects of the main hemostasis protease, thrombin, on the state of brain glial cells under conditions of oxygen-glucose deprivation and subsequent normoxia ("ischemia/reperfusion" model) were estimated. It was found that thrombin in low concentrations (10 nM) has a protective effect on rat astrocytes during ischemia/reperfusion. Pre-incubation of astrocytes with a low concentration of protease caused an increase in cell survival under these conditions, while an increase in the concentration (50 nM) reduced its protective effect. It was revealed that thrombin in both concentrations does not affect the proliferation of astrocytes induced by ischemia/reperfusion. It was shown that oxygen-glucose deprivation leads to the redistribution of actin filaments in astrocytes from under the membrane space to the region of the cell nucleus. Thrombin in high concentration potentiated the effect of oxygen-glucose deprivation on the actin cytoskeleton of astrocytes. Thus, the nature of the effect of thrombin on cerebral astrocytes during oxygen-glucose deprivation and subsequent reperfusion is dose-dependent.