Influence of Naomai II capsule on dynamic expression of protease-activated receptors-1 after acute intracerebral hemorrhage.
- Author:
Guo-qing ZHENG
1
;
Pei-xin HUANG
Author Information
- Publication Type:Journal Article
- MeSH: Acute Disease; Animals; Capsules; Cerebral Hemorrhage; metabolism; Drug Combinations; Drugs, Chinese Herbal; administration & dosage; isolation & purification; pharmacology; Male; Materia Medica; administration & dosage; pharmacology; Plants, Medicinal; chemistry; RNA, Messenger; biosynthesis; genetics; Random Allocation; Rats; Rats, Wistar; Receptor, PAR-1; biosynthesis; genetics
- From: China Journal of Chinese Materia Medica 2006;31(15):1265-1268
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo 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.
METHOD72 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.
RESULTPAR-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).
CONCLUSIONAfter 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.