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

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