Role of thrombin receptor in the pathogenesis of cerebral hemorrhage in rats
Chang Cheng, Tcm Hosptial
Abstract
Chang Cheng, Tcm Hosptial
Abstract
Objective To investigate the expression of thrombin receptor 1 (PAR1) and its role in the pathogenesis of intracerebral hemorrhage (ICH).Methods The adult rats were divided into three groups,and intracerebrally given with autologous whole blood (50μl),autologous blood plus hirudin thrombin solution (10 units),or normal saline (NS),respectively.At 6,24,72 hours and 7days after injection, the brains were taken out for detecting the PAR1 expression (Immunostaining method) and the apoptosis cell (Tunel method).The water content of brains was also assayed.Results The number of positive PAR1-immunostaining cells in the tissue surrounding hemotoma were markedly increased at 6h after ICH,peaked at 72h and decreased at 7d after ICH.At the same time,the apoptosis cells and brain water contents were also increased. However PAR1 expression, apoptotic cells and brain water content were markedly inhibited in cases of coinjection of Hirudin and blood.Conclusion PAR1 expression was upregulated during ICH.The activation of PAR1 might be involved in the pathogenesis of ICH.
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Objective To investigate the expression of thrombin receptor 1 (PAR1) and its role in the pathogenesis of intracerebral hemorrhage (ICH).Methods The adult rats were divided into three groups,and intracerebrally given with autologous whole blood (50μl),autologous blood plus hirudin thrombin solution (10 units),or normal saline (NS),respectively.At 6,24,72 hours and 7days after injection, the brains were taken out for detecting the PAR1 expression (Immunostaining method) and the apoptosis cell (Tunel method).The water content of brains was also assayed.Results The number of positive PAR1-immunostaining cells in the tissue surrounding hemotoma were markedly increased at 6h after ICH,peaked at 72h and decreased at 7d after ICH.At the same time,the apoptosis cells and brain water contents were also increased. However PAR1 expression, apoptotic cells and brain water content were markedly inhibited in cases of coinjection of Hirudin and blood.Conclusion PAR1 expression was upregulated during ICH.The activation of PAR1 might be involved in the pathogenesis of ICH.
Key concepts: Pathogenesis, Immunostaining, Intracerebral hemorrhage, Apoptosis, Hirudin, TUNEL assay, Thrombin, Thrombin receptor