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

您当前的位置：

首页 >

文章列表页 >

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
- Published：20 September 2019，
  
  Published Online：04 June 2019，
  
  Received：13 March 2019，
- 稿件说明：
扫描看全文
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 25(18):30-35(2019)
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 25(18):30-35(2019) 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

清金化痰汤慢性阻塞性肺疾病(COPD)自噬

Keywords

Qingjin Huatan Tang (QJHTD)chronic obstructive pulmonary disease (COPD)autophagy

references

中华医学会呼吸病学分会慢性阻塞性肺疾病学组．慢性阻塞性肺疾病诊治指南(2013 年修订版)[J]，中国医学前沿杂志：电子版，2014，6(2)，68-79．

Russell K E, Chung K F, Clarke C J, et al. The MIF antagonist ISO-1 attenuates corticosteroid-insensitive inflammation and airways hyperresponsiveness in an ozone-induced model of COPD [J].PLoS One, 2016, 11: e0146102.

Husebo G R, Bakke P S, Gronseth R, et al. Macrophage migration inhibitory factor, a role in COPD [J].Am J Physiol Lung Cell Mol Physiol, 2016, 311: L1-L7.

Saitoh T, Fujita N, Jang M H, et al. Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1β production [J].Nature, 2008, 456(7219): 264-268.

许光兰，赵媚，钟云青，等．清金化痰颗粒对COPD急性期(痰热郁肺型)大鼠肺组织STAT1，STAT3的调控作用[J]．中国实验方剂学杂志，2017，23(2)：91-97．

许光兰，李国生．清热化痰法在慢性阻塞性肺疾病急性加重期中的应用研究[J]．时珍国医国药，2018，29(4)：950-952．

王骏，李春盈，刘治坤，等．慢性阻塞性肺疾病气道粘液高分泌大鼠模型的建立[J]．心肺血管病杂志，2014，33(4)：592-595．

尚立芝，谢文英，张良芝，等．爱罗咳喘宁对慢性阻塞性肺疾病大鼠白三烯B4、白细胞介素-6及肺组织病理形态的影响[J]．中国实验方剂学杂志，2014，20(12)：170-173．

鹿振辉．中医药对COPD多靶点作用的研究进展[J]．江苏中医，2006，27(7)：61-63．

邹琴，王博龙．长期小剂量罗红霉素对稳定期慢性阻塞性肺疾病疗效作用的Meta分析[J]．中国抗生素杂志，2018，43(10)：1312-1320．

卫娜，王晓晓，王映棋，等．玉屏风散加味方对慢性阻塞性肺疾病大鼠气道炎症微环境的影响[J]．现代中西医结合杂志，2018，27(5)：457-461．

朱静，尚广彬，张洁，等．自噬在中医药治疗肿瘤中的研究进展[J]．中国实验方剂学杂志，2019，doi: 10.13422/j.cnki.syfjx.20191321http://doi.org/10.13422/j.cnki.syfjx.20191321．

李欢，苗明三．自噬及中医药调控自噬在治疗和防治疾病中的研究进展[J]．中国实验方剂学杂志，2018，24(20)：200-207．

YAO H, Rahman I. Current concepts on oxidative/carbonyl stress, inflammation and epigenetics in pathogenesis of chronic obstructive pulmonary disease [J].Toxicol Appl Pharmacol, 2011, 254(2): 72-85.

Vogelmeier F C, Criner J G, Martinez J F, et al. Global strategy for the diagnosis, management and prevention of chronic obstructive lung disease 2017 report [J].Respirology, 2017, 22(3): 575-601.

Bodas M, Patel N, Silverberg D, et al. Master autophagy regulator Transcription factor-EB (TFEB) regulates cigarette smoke induced autophagy-impairment and COPD-emphysema pathogenesis [J].Antioxid Redox Signal, 2017, doi: 10.1089/ars.2016.6842http://doi.org/10.1089/ars.2016.6842.

Roscioli E, Hamon R, Lester S E, et al. Airway epithelial cells exposed to wildfire smoke extract exhibit dysregulated autophagy and barrier dysfunction consistent with COPD [J].Respir Res, 2018, 19(1): 234.

Jeffrey A H, Augustine M K. Autophagy A core cellular process with emerging links to pulmonary disease [J].Am J Respir Crit Care Med, 2011, 184, 1066: 259-271.

陈丹丹，彭成，李梦婷，等．自噬参与氢溴酸樟柳碱对缺氧状态下PC12细胞损伤的保护作用[J]．中国实验方剂学杂志，2017，23(20)：144-149．

刘晨阳，白宽，于顾然．梓醇对纤维状Aβ1-42诱导的bEnd.3细胞凋亡及过度自噬的影响[J]．中国实验方剂学杂志，2017，23(20)：108-113．

Beth L, Noboru M, Herbert W V. Autophagy in immunity and inflammation [J].Nature, 2011, 469(7330): 323-335.

Hwang J W, Sangwoon C, Isaac K, et al. Cigarette smoke-induced autophagy is regulated by SIRT1-PARP-1-dependent mechanism: implication in pathogenesis of COPD [J].Arch Biochem Biophys, 2010, 500: 203-209.

Deretic V. Autophagy as an innate immunity paradigm: expanding the scope and repertoire of pattern recognition receptor [J].Curr Opin Immunol, 2012, 24(1): 21-31.

Nakahira K. Autophagy: a crucial moderator of redox balance, inflammation, and apoptosis in lung disease [J].Antioxid Redox Signal, 2014, 20(3): 474-494.

Hammada D R, Elgazzara A G, Essawya T S, et al. Evaluation of serum interleukin-1 beta as an inflammatory marker in COPD patients [J].Egyptian J Chest Dis Tuberc, 2015, 64: 347-352.

Jae W H, Sangwoon C, Isaac K S, et al. Cigarette smoke inducedautophagy is regulated by SIRT1-PAPR-1-dependent mechanism: implication in pathogenesis of COPD [J].Arch Biochem Biophys, 2010, 500(2): 203-209.

Monick M M, Powers L S, Walters K, et al. Identification of an autophagy defect in smokers'' alveolar macrophages [J].J Immunol, 2010, 185(9): 5425-5435.

Views

下载量

CSCD

Alert me when the article has been cited

提交

Tools

Publicity Resources

Effect of Huangjingwan on Hippocampal Autophagy in Mouse Model of Learning and Memory Impairments

Role of Autophagy in Ovarian Cancer Based on Yin and Yang Theory

Icariin Regulates Glucocorticoid-induced Autophagy of Bone Microvascular Endothelial Cells Through PI3K/Akt/mTOR Pathway

Effect of Buyang Huanwutang in Treating Diabetic Peripheral Neuropathy by Inhibiting Pyroptosis Through AMPK/ULK1 Mitophagy Pathway

Qidi Tangshen Prescription （QDTS） Regulate Akt1/HIF-1α/Bcl-xl Signaling Pathway to Improve Podocyte Autophagy in Diabetic Nephropathy

Related Author

LIAO Kexin

JIANG Jielin

XIAO Yisheng

PENG Cheng

GUO Ying

YU Yang

LIU Fangyuan

HAN Fengjuan

Related Institution

College of Chinese Medicine， Jiangxi University of Chinese Medicine

Heilongjiang University of Chinese Medicine

The First Affiliated Hospital of Heilongjiang University of Chinese Medicine

Graduate School， Beijing University of Chinese Medicine

Peking University Health Science Center

Postal code：100700
Tel：010-84076882 Email：syfjx_2010@188.com
Technical support is provided by Beijing Founder electronics co., LTD 京ICP备11006657号-10 京公网安备11010802024621
It is recommended to read the content of this site in Chrome&IE9+. Please switch to extreme mode in browser 360.
Cookies We use cookies to help provide and enhance our service and tailor content. By continuing, you agree to the use of cookies.

⁰