2005Chinese journal of integrated traditional and Western medicineRequires access

Influence of Naoxuekang on expression of proteaseactivated receptor1 in rats with intracerebral hemorrhage

Peixin Huang

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Abstract

Objective: To investigate the dynamic expression of proteaseactivated receptor1 (PAR1) after intracerebral hemorrhage (ICH) and the intervention effects of Naoxuekang (NXK) on the expression. Methods: Seventytwo rats were randomly divided into normal group, ICH model groups (ICH 6 hours, 24 hours, 3 days, 7 days), Naoxuekang treatment groups (NXK, 6 hours, 24 hours, 3 days, 7 days). ICH models were reproduced with induction of collagenase type ⅦS in the rats. PAR1 protein was detected by immunohistochemical method and PAR1 mRNA was detected by reverse transcriptionpolymerase chain reaction (RTPCR) technique in brain tissue around the haematoma at different time points in different groups. Results: PAR1 protein and mRNA were mildly positive in normal group. In model groups, intensity of PAR1 expression began to enhance at 6 hours, and enhanced more at 24 hours, peaking at 3 days, then declined, and was obvious at 7 days. At 6 hours, 24 hours, 3 days and 7 days, the increase of PAR1 protein positive cells and PAR1 mRNA optical density (A value) in rats of NXK treatment groups and ICH model groups were significant, compared to those of the normal group (P0.05 or P0.01). The decrease of PAR1 protein positive cells and PAR1 mRNA A value in rats of NXK treatment groups were more significant, compared to those of the rats in ICH model groups (P0.05 or P0.01). Conclusion: After ICH, PAR1 is continuously activated by the stimulation of thrombin. The function of thrombin after ICH may be mediated by PAR1. NXK may improve praxiology by inhibiting the activation of PAR1. It may be one of the main mechanisms of NXK facilitating the recovery of nervous function.

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Objective: To investigate the dynamic expression of proteaseactivated receptor1 (PAR1) after intracerebral hemorrhage (ICH) and the intervention effects of Naoxuekang (NXK) on the expression. Methods: Seventytwo rats were randomly divided into normal group, ICH model groups (ICH 6 hours, 24 hours, 3 days, 7 days), Naoxuekang treatment groups (NXK, 6 hours, 24 hours, 3 days, 7 days). ICH models were reproduced with induction of collagenase type ⅦS in the rats. PAR1 protein was detected by immunohistochemical method and PAR1 mRNA was detected by reverse transcriptionpolymerase chain reaction (RTPCR) technique in brain tissue around the haematoma at different time points in different groups. Results: PAR1 protein and mRNA were mildly positive in normal group. In model groups, intensity of PAR1 expression began to enhance at 6 hours, and enhanced more at 24 hours, peaking at 3 days, then declined, and was obvious at 7 days. At 6 hours, 24 hours, 3 days and 7 days, the increase of PAR1 protein positive cells and PAR1 mRNA optical density (A value) in rats of NXK treatment groups and ICH model groups were significant, compared to those of the normal group (P0.05 or P0.01). The decrease of PAR1 protein positive cells and PAR1 mRNA A value in rats of NXK treatment groups were more significant, compared to those of the rats in ICH model groups (P0.05 or P0.01). Conclusion: After ICH, PAR1 is continuously activated by the stimulation of thrombin. The function of thrombin after ICH may be mediated by PAR1. NXK may improve praxiology by inhibiting the activation of PAR1. It may be one of the main mechanisms of NXK facilitating the recovery of nervous function.

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Available abstract

Objective: To investigate the dynamic expression of proteaseactivated receptor1 (PAR1) after intracerebral hemorrhage (ICH) and the intervention effects of Naoxuekang (NXK) on the expression. Methods: Seventytwo rats were randomly divided into normal group, ICH model groups (ICH 6 hours, 24 hours, 3 days, 7 days), Naoxuekang treatment groups (NXK, 6 hours, 24 hours, 3 days, 7 days). ICH models were reproduced with induction of collagenase type ⅦS in the rats. PAR1 protein was detected by immunohistochemical method and PAR1 mRNA was detected by reverse transcriptionpolymerase chain reaction (RTPCR) technique in brain tissue around the haematoma at different time points in different groups. Results: PAR1 protein and mRNA were mildly positive in normal group. In model groups, intensity of PAR1 expression began to enhance at 6 hours, and enhanced more at 24 hours, peaking at 3 days, then declined, and was obvious at 7 days. At 6 hours, 24 hours, 3 days and 7 days, the increase of PAR1 protein positive cells and PAR1 mRNA optical density (A value) in rats of NXK treatment groups and ICH model groups were significant, compared to those of the normal group (P0.05 or P0.01). The decrease of PAR1 protein positive cells and PAR1 mRNA A value in rats of NXK treatment groups were more significant, compared to those of the rats in ICH model groups (P0.05 or P0.01). Conclusion: After ICH, PAR1 is continuously activated by the stimulation of thrombin. The function of thrombin after ICH may be mediated by PAR1. NXK may improve praxiology by inhibiting the activation of PAR1. It may be one of the main mechanisms of NXK facilitating the recovery of nervous function.

Key concepts: Intracerebral hemorrhage, Messenger RNA, Medicine, Thrombin, Immunohistochemistry, Collagenase, Stimulation, Rat model

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