Effect of Qingjin Huatan Tang on COPD of Rat Inflammatory Response by Regulating Autophagy

Lin-na WU; Mei ZHAO; Guang-lan XU

doi:10.13422/j.cnki.syfjx.20191801

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Effect of Qingjin Huatan Tang on COPD of Rat Inflammatory Response by Regulating Autophagy

Classic Prescriptions | 更新时间：2021-02-09

- Effect of Qingjin Huatan Tang on COPD of Rat Inflammatory Response by Regulating Autophagy
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 25, Issue 18, Pages: 30-35(2019)
- 作者机构：
  
  广西中医药大学　第一附属医院，南宁　 530023
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20191801
  CLC： R2-0; R22; R285.5; R289
- Received：13 March 2019，
  
  Published Online：04 June 2019，
  
  Published：20 September 2019
- 稿件说明：
移动端阅览
Lin-na WU, Mei ZHAO, Guang-lan XU. Effect of Qingjin Huatan Tang on COPD of Rat Inflammatory Response by Regulating Autophagy[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(18): 30-35.
DOI：

Lin-na WU, Mei ZHAO, Guang-lan XU. Effect of Qingjin Huatan Tang on COPD of Rat Inflammatory Response by Regulating Autophagy[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(18): 30-35. DOI： 10.13422/j.cnki.syfjx.20191801.

摘要

目的：

通过观察清金化痰汤对慢性阻塞性肺疾病(COPD)大鼠的自噬调节作用，探讨其对COPD大鼠的炎症反应的影响。

方法：

采用50只SPF级雄性SD大鼠随机分成5组，分别为正常组、模型组、清金化痰汤高、低剂量组(30，10 g·kg

－1

)，罗红霉素组(0.017 5 g·kg

－1

)，每组10只，除正常组10只外，余40只用单纯烟熏方法建立COPD大鼠动物模型28 d。苏木素-伊红(HE)染色鉴定模型成立后，5组分别灌胃给药14 d，1次/d，模型组、正常组同体积生理盐水灌胃。末次灌胃1 h后处死大鼠提取气道，采用实时荧光定量聚合酶链式反应(Real-time PCR)，蛋白免疫印迹法(Western blot)检测其自噬相关蛋白微管相关蛋白轻链3(LC3)，Beclin-1表达；酶联免疫吸附测定(ELISA)检测炎症因子白细胞介素-6(IL-6)，IL-8的含量变化。

结果：

Real-time PCR分析显示，与正常组比较，模型组自噬因子Beclin-1，LC3 mRNA表达均有不同程度升高(

0.05)；与模型组比较，清金化痰汤处理后能够明显改善COPD大鼠气道上皮细胞自噬反应，自噬表达明显减少(

0.05)，高剂量组与罗红霉素组比较差异不显著。Western blot结果显示，与正常组比较，模型组自噬蛋白表达明显升高(

0.05)；与模型组比较，清金化痰汤药物处理组自噬蛋白Beclin-1，LC3表达下降(

0.05)；清金化痰汤高剂量组与罗红霉素组比较差异不显著。ELISA结果显示，模型组大鼠的炎症水平升高，用药处理后大鼠气道上皮细胞内的炎症因子IL-6，IL-8含量均明显下降(

0.05)。

结论：

清金化痰汤能够减轻COPD大鼠支气管的炎症反应，其机制可能与清金化痰汤抑制气道上皮的自噬水平有关。

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(

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 (

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 (

0.05). compared with model control group

autophagy protein Beclin 1

LC3 expressions of the QJHTD treatment group were decreased (

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 (

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.

关键词

Keywords

references

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