Effect of Qingjin Huatan Tang on COPD of Rat Inflammatory Response by Regulating Autophagy
10.13422/j.cnki.syfjx.20191801
- VernacularTitle: 清金化痰汤通过调节自噬对COPD大鼠炎症反应的影响
- Author:
Lin-na WU
1
;
Mei ZHAO
1
;
Guang-lan XU
1
Author Information
1. The First Affiliated Hospital of Guangxi University of Traditional Chinese Medicine, Nanning 530023, China
- Publication Type:Research Article
- Keywords:
Qingjin Huatan Tang (QJHTD);
chronic obstructive pulmonary disease (COPD);
autophagy
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2019;25(18):30-35
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To explore the effect of Qingjin Huatan Tang (QJHTD) on the inflammatory response of chronic obstructive pulmonary disease(COPD) rats by observing the autophagy regulating effect of QJHTD on COPD rats. Method: The 50 SPF grade male rats were randomly divided into 5 groups, with 10 rats in each group. In addition to the normal group, the remaining 40 male rats were randomly divided into 5 groups. After the establishment of the hematoxylin and eosin(HE) staining identification model, the drugs were given to the 5 groups by gavage for 2 weeks, high and low-dose QJHTD groups were give the drug at 30, 10 g·kg-1. Roxithromycin positive control group was given the drug at 0.017 5 g·kg-1. The model control group and the normal group were given the same volume of normal saline. At 1 h after the last gavage, the rats were put to death to extract the airway, and the expressions of autophagy microtuble-associated protein light chain 3 (LC3),Beclin-1 were detected by Real-time quantitative PCR (Real-time PCR) and Western blot. Changes of inflammatory cytokines interleukin-6 (IL-6) and interleukin-8(IL-8) were detected by enzyme linked immunosorbent assay (ELISA). Result: Real-time PCR analysis showed that compared with the normal group, Beclin-1 and LC3 mRNA expressions of autophagy factors in the model group were increased to varying degrees(P<0.05). QJHTD could significantly improve the autophagy response of airway epithelial cells in COPD rats, and the autophagy expression was significantly reduced compared with the model control group (P<0.05), with no significant difference between the high-dose group and the positive control group. Western blot results show that compared with the normal group, the expression of autophagy protein in the model group was significantly increased (P<0.05). compared with model control group, autophagy protein Beclin 1, LC3 expressions of the QJHTD treatment group were decreased (P<0.05). There was no significant difference between the high-dose QJHTD group and the Roxithromycin positive control group. ELISA results showed that the inflammatory level of mice in the model group was increased, while the contents of inflammatory cytokines IL-6 and IL-8 in the airway epithelial cells of mice were decreased after treatment (P<0.05). Conclusion: QJHTD can alleviate the bronchial inflammation in COPD rats, and its mechanism may be related to the inhibition of autophagy in airway epithelium by QJHTD.
