[Complement componenets, C3 and factors B, in the blood of patients with acute ischemic stroke].

Several studies suggest that activation of compliment cascade contributes to the development of the inflammatory immune response in ischemic stroke and results in tissue injury by initiating apoptosis and necrosis. It is proposed that suppression of the compliment activation may have positive effect on stroke severity and outcome. However, the majority of data relevant to involvement of the compliment in the pathogenethic mechanisms of stroke have been obtained in animal models of stroke that does not allow to extrapolate these data to humans. Our previous studies were the first ones demonstrated the involvement of both the classical and the alternative complement activation pathways in the pathogenetic mechanisms of generation and development of stroke in humans. In the present work, using immunoblotting, we determined the levels of key components of the classical and alternative pathways of complement activation, C3 and factor B, in the blood of patients with ischemic stroke. Comparing to healthy controls, patients with ischemic stroke are characterized by the increased level of C3 and decreased level of factor B.