Effect of Ailuo Kechuanning on Expression of p38MAPK, TNF- and AQP5 Genes in Rats with Chronic Obstructive Pulmonary Disease

SHANG Li-zhi; XIE Wen-ying; ZHANG Liang-zhi; CHANG Xue-hui; PAN Xiao-li; HU Wen-hao; LIU Tan

doi:10.13422/j.cnki.syfjx.2014230174

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Effect of Ailuo Kechuanning on Expression of p38MAPK, TNF- and AQP5 Genes in Rats with Chronic Obstructive Pulmonary Disease

更新时间：2024-01-04

- Effect of Ailuo Kechuanning on Expression of p38MAPK, TNF- and AQP5 Genes in Rats with Chronic Obstructive Pulmonary Disease
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 20, Issue 23, Pages: 174-179(2014)
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.2014230174
  CLC： R285.5
- Published：2014
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SHANG Li-zhi, XIE Wen-ying, ZHANG Liang-zhi, et al. Effect of Ailuo Kechuanning on Expression of p38MAPK, TNF- and AQP5 Genes in Rats with Chronic Obstructive Pulmonary Disease[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(23): 174-179.
DOI：

SHANG Li-zhi, XIE Wen-ying, ZHANG Liang-zhi, et al. Effect of Ailuo Kechuanning on Expression of p38MAPK, TNF- and AQP5 Genes in Rats with Chronic Obstructive Pulmonary Disease[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(23): 174-179. DOI： 10.13422/j.cnki.syfjx.2014230174.

摘要

目的: 观察爱罗咳喘宁对慢性阻塞性肺疾病(chronic obstructive pulmonarydisease

COPD)大鼠模型支气管和肺组织中p38丝裂原活化蛋白激酶(p38mitogen activatein kinase

p38MAPK)、肿瘤坏死因子-α(tumor necrosis factor alpha

TNF-α)、及水通道蛋白5(aquaporin 5

AQP5)基因表达的影响

探讨爱罗咳喘宁方对COPD炎症及气道高分泌的作用及机制. 方法: 采用脂多糖(lipopolysaccharide

LPS)加烟雾诱导COPD大鼠模型

随机将大鼠分为正常组、模型组、爱罗咳喘宁低、中、高剂量组.正常组、模型组灌胃生理盐水(15.52 mL·kg-1·d-1)

爱罗咳喘宁口服液低、中、高剂量组分别灌胃(7.75

15.52

31.04 g·kg-1·d-1)

连续15 d.原位杂交、免疫组化检测p38MAPK、TNF-α及AQP5基因在细支气管和肺组织中的原位表达. 结果: 与正常对照组比较

模型组大鼠AQP5 mRNA[(4.52±0.11)VS(0.87±0.32)

P<0.01]和蛋白[(3.98±0.22)VS(0.58±0.02)

P<0.01]表达均显著减弱

而p38MAPK mRNA[(0.49±0.02)VS(0.85±0.02)

P<0.01]

TNF-α mRNA[(0.26±0.01)VS(0.44±0.01)

P<0.01]均显著增强

p-p38MAPK蛋白[(0.30±0.01)VS(0.41±0.01)

P<0.05]和TNF-α蛋白[(0.20±0.01VS(0.38±0.01)

P<0.05]表达均显著增强

AQP5蛋白与p-p38MAPK

TNF-α蛋白表达均呈负相关(r分别为-0.547

-0.532

P<0.01);与模型组相比

爱罗咳喘宁中剂量组AQP5 mRNA[(0.87±0.32 VS 1.80±0.32

P<0.01)]

AQP5蛋白[(0.58±0.02 VS 1.61±0.72

P<0.01)]表达显著增强

p38MAPK mRNA[(0.85±0.02)VS(0.51±0.02)

P<0.01]

TNF-α mRNA[(0.44±0.01)VS(0.40±0.01)

P<0.01]表达减弱

p38MAPK蛋白[(0.41±0.01)VS(0.32±0.00)

P<0.01]TNF-α蛋白[(0.38±0.01)VS(0.31±0.00)

P<0.01]表达显著减弱.AQP5蛋白表达与p-P38MAPK

TNF-α蛋白均呈显著负相关(r分别为-0.542

-0.541

均P<0.01). 结论: 爱罗咳喘宁有抗炎和抑制COPD气道黏液高分泌作用

其机制可能与下调p38MAPK

TNF-α基因表达、上调AQP5基因表达有关.

Abstract

Objective: To study the effect of Ailuo Kechuanning on expression of p38MAPK

tumor necrosis factor alpha(TNF-α)

and aquaporin 5(AQP5) genes in rats with chronic obstructive pulmonary disease(COPD). Method: Lipopolysaccharide(LPS)smoke was used to COPD rat model

the experimental animals were randomly divided into normal control group

model group

Normal group

model group was given physiological saline(15.52 mL· kg-1· d-1) byintragastric

Ailuo Kechuanning group(7.75

15.52

31.04 g· kg-1· d-1)

ig for 15 days. The expression of p38MAPK

TNF-α and AQP5 genes in the trachea

bronchus and lung tissue were detected by in situ hybridization and immunohistochemical techniques. Result: Compared with the normal group

the expression of mRNA and protein of AQP5 were weakened

but the expression of p38MAPK

TNF-α mRNA and protein were enhanced in model group

the expression of AQP5 protein was negatively correlated with p38MAPK(r=-0.547

P<0.01)

TNF-α protein(r=-0.532

P<0.01).Compared Ailuo Kechuanning mediate-dose group with the model group

the expression of AQP5 gene in enhancements

However

the expression of p38MAPK

TNF-α genes was decreased apparently

the expression of AQP5 protein was negatively correlated with p38MAPK(r=-0.542

P<0.01)

TNF-α protein(r=-0.541

P<0.01). Conclusion: The mechanism of Ailuo Kechuanning regulating COPD airway mucus hypersecretion may increase AQP5 gene and inhibit p38 MAPK

TNF-α genes expression.

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