Zheng Guo-qing, Huang Pei-xin
Center of Neurology, Second Affiliated Hospital of Wenzhou Medical College, China.
Zhongguo Zhong Yao Za Zhi. 2006 Aug;31(15):1265-8.
To study the dynamic expression of protease-activated receptor-1(PAR-1) after acute intracerebral hemorrhage (ICH) and the influence of Naomai capsule (NMC II) on the expression in rats.
72 rats were randomly divided into 9 groups (n = 8 in each group). They were normal group, ICH model groups at 6, 24 h, 3, 7 d and NMC II groups at 6, 24 h, 3, 7 d. ICH models were induced by collagenase type VII-S. Immunohistochemical method was used to detect PAR-1 protein and RT-PCR technique was used to detect PAR-1mRNA in brain tissue around the haematoma at different groups.
PAR-1 protein and mRNA were mild positive in normal group. In model groups, intensity of PAR-1 expression started to enhance at 6 h, and enhanced more at 24 h. PAR-1 expression reached the peak at 3 d and began to descend. At 7 d the decent was obvious. At 6, 24 h, 3, 7 d time point. The PAR-1 protein positive cell number and PAR-1 mRNA absorbance ratio in ICH model and NMC II groups were significantly higher than those in normal group (P < 0.05 or P < 0.01). The PAR-1 protein positive cell number and PAR-1mRNA absorbance ratio in NMC II group were significantly lower than those in ICH model group (P < 0.05 or P < 0.01).
After ICH, PAR-1 is continuously activated because of the simulation of thrombin. Function of thrombin after ICH maybe mediated by PAR-1; NMC II may inhibit the expression of PAR-1. This may be one of the main therapeutics mechanisms of NMC II.
研究急性脑出血(ICH)后蛋白酶激活受体-1(PAR-1)的动态表达及脑脉胶囊(NMC II)对大鼠PAR-1表达的影响。
将72只大鼠随机分为9组(每组n = 8)。分别为正常组、ICH模型6小时、24小时、3天、7天组以及NMC II 6小时、24小时、3天、7天组。采用VII-S型胶原酶诱导建立ICH模型。采用免疫组织化学方法检测不同组血肿周围脑组织中PAR-1蛋白,采用RT-PCR技术检测PAR-1mRNA。
正常组PAR-1蛋白和mRNA呈轻度阳性。模型组中,PAR-1表达强度在6小时开始增强,24小时增强更明显。PAR-1表达在3天达到峰值并开始下降。在7天时下降明显。在6小时、24小时、3天、7天时间点,ICH模型组和NMC II组的PAR-1蛋白阳性细胞数及PAR-1mRNA吸光度比值均显著高于正常组(P < 0.05或P < 0.01)。NMC II组的PAR-1蛋白阳性细胞数及PAR-1mRNA吸光度比值显著低于ICH模型组(P < 0.05或P < 0.01)。
ICH后,由于凝血酶的刺激,PAR-1被持续激活。ICH后凝血酶的作用可能由PAR-1介导;NMC II可能抑制PAR-1的表达。这可能是NMC II主要治疗机制之一。