Influence of Nao Xue Kang tablet on dynamic expression of PAR- 1after acute intracerebral hemorrhage in rats
- VernacularTitle:脑血康片对急性脑出血大鼠PAR-1表达及动态演变的影响
- Author:
Guoqing ZHENG
;
Yan WANG
;
Xiaotong WANG
- Publication Type:Journal Article
- Keywords:
Cerebral hemorrhage;
Nao Xue Kang tablet;
Thrombin;
Protease- activated receptors- 1
- From:
Chinese Journal of Pathophysiology
2006;22(4):786-790
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To study the dynamic expression of protease - activated receptors - 1 (PAR- 1 ) after intracerebral hemorrhage (ICH) and the influence of Nao Xue Kang Tablet (NXKT) on it's expression. METHODS: 72 Wistar rats were divided into normal group, ICH model groups (ICH, 6 h, 24 h, 3 d, 7 d), Nao Xue Kang groups (NXKT, 6 h, 24 h, 3 d,7 d).ICH models were produced with the induction of collagenase typeⅦ - S, except normal group. Immunohistochemical method was used to detect PAR- 1 protein and RT- PCR technique was used to detect PAR- 1 mRNA in brain tissues around the haematoma at different time points of different groups. RESULTS: PAR - 1 protein and mRNA were mildly positive in normal group. In ICH model groups, intensity of PAR - 1 expression started to increase at 6 h, and further increased 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 h, 24 h, 3 d, and 7 d time points, the PAR-1 protein positive cell number and PAR- 1 mRNA absorbance ratio in ICH model and NXKT 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- 1 mRNA absorbance ratio in NXKT group were significantly lower than in ICH model group ( P ＜ 0.05 or P ＜ 0.01 ). CONCLUSION: After ICH,PAR - 1 is continuously activated because of the stimulation of thrombin. Action of thrombin after ICH may be mediated by PAR- 1; NXKT may inhibit the activation of PAR- 1, so the praxiology is improved. This may be one of the main mechanisms that NXKT could facilitate the recovery of nervous function.
