Mechanism of JinShuiBao capsule in ameliorating rat pneumoconiosis model
10.11665/j.issn.1000-5048.20180414
- VernacularTitle:金水宝胶囊对尘肺模型大鼠的改善作用及其机制
- Author:
Wei LIU
1
;
Shufan JIANG
;
Lei TU
;
Weiyi HU
;
Tao WANG
;
Jing. WANG
Author Information
1. 南京市职业病防治院药剂科
- Publication Type:Journal Article
- Keywords:
JinShuiBao capsule;
pneumoconiosis;
pulmonary fibrosis;
mechanism of action;
immune regulation;
hemorrheology
- From:
Journal of China Pharmaceutical University
2018;49(4):476-482
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the mechanism of JinShuiBao capsule on improving respiratory function and lung tissue pathology in rat pneumoconiosis model. Chronic pneumoconiosis rat model was established by tracheal injection of quartz dust. JinShuiBao was administrated orally by 600 and 300 mg/kg, once daily for 6 months. At the 1st, 3rd and 6th month of administration, 6 rats in each group were taken for hemorheology, vascular endothelial function, immunoinflammatory cytokines and oxidative stress. The results showed that high dose of JinShuiBao had a significant improvement on the plasma viscosity at each time point(P< 0. 05)during the 6-month trial, and partially improved the whole blood viscosity. Both dose of JinShuiBao capsule significantly decreased the levels of serum inflammatory cytokines such as TGF-β, TNF-α and IL-6(P< 0. 05, P< 0. 01), and high dose group could significantly decrease the level of CD4+/CD8+(P< 0. 01). The high dosage of JinShuiBao could obviously reduce the level of serum MDA and increase the activity of SOD(P< 0. 05), and obviously reduced the number of leukocytes in the bronchoalveolar lavage fluid of model rats. In the high-dose group, the levels of ET, NO and PC in bronchoalveolar lavage fluid were significantly improved in all the experimental periods(P< 0. 05, P< 0. 01), while the low-dose group also had a statistically significant improvement at 3 month later. These results suggested that the improvement of JinShuiBao capsule on pneumoconiosis rats involved various mechanism, including blood viscosity, systemic and pulmonary inflammatory response, vascular endothelial injury, and oxidative stress in the whole body and lung fibrosis.
