Effect of Da Jianzhong Decoction on Cyclooxygenase-2 mRNA and Protein and Calmodulin-dependent Protein KinaseⅡmRNA in Spleen-yang Deficiency Pain Rats
10.13359/j.cnki.gzxbtcm.2016.01.018
- VernacularTitle:大建中汤对脾阳虚疼痛大鼠COX-2 mRNA及蛋白和CaMKⅡmRNA的影响
- Author:
Jing WU
- Publication Type:Journal Article
- Keywords:
Da Jianzhong Decoction/pharmacology;
spleen-yang deficiency pain/TCD therapy;
brain/pathology;
gene expression regulation;
protein expression;
disease models,animal;
rats
- From:
Journal of Guangzhou University of Traditional Chinese Medicine
2016;(1):71-75
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect of Da Jianzhong Decoction on cerebral cyclooxygenase-2 (COX-2) mRNA and protein and calmodulin-dependent protein kinase II(CaMKⅡ) mRNA in spleen-yang deficiency pain rats, so as to investigate the therapeutic mechanism of Da Jianzhong Decoction for spleen-yang deficiency pain. Methods Forty SD rats were randomly divided into normal group, model group, and high-and low-dose Da Jianzhong Decoction groups(3, 0.75 g·kg-1·d-1), 10 in each group. Spleen deficiency rat model was established by comprehensive modeling methods. After the rats in various groups were given gastric administration of Chinese medicine for 15 continuous days, rat cervical dislocation was performed for the sampling of the brain tissue. The expression levels of COX-2 mRNA and CaMKⅡmRNA in brain tissue were detected by real time polymerase chain reaction (RT-PCR). The COX-2 protein expression was determined by immunohistochemistry. Results Compared with the normal group, mRNA and protein expression levels of COX-2 in rat brain tissue of spleen-yang deficiency model group were increased(P﹤0.01), and CaMKⅡ mRNA expression was decreased (P<0.01). Compared with the model group, COX-2 mRNA and protein expression levels were decreased(P<0.01) and CaMKⅡexpression was increased(P<0.01) in high-and low-dose Da Jianzhong Decoction groups(P<0.01). Conclusion Da Jianzhong Decoction can suppress cerebral COX-2 mRNA and protein expression, and up-regulate CaMKⅡmRNA expression, which probably contribute to its therapeutic mechanism for relieving the pain.
