Anti-inflammatory Mechanism of Qishe Pill in vitro

PAN Yi-feng1; YANG Xiao-lu2; WANG Jian-qiang1; ZHANG Dan-dan2

doi:10.13422/j.cnki.syfjx.2012.18.055

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Anti-inflammatory Mechanism of Qishe Pill in vitro

更新时间：2024-09-23

- Anti-inflammatory Mechanism of Qishe Pill in vitro
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 18, Issue 18, Pages: 144-147(2012)
- 作者机构：
  
  1. 上海现代中医药股份有限公司
  2. 上海中医药大学穆拉德中药现代化研究中心
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.2012.18.055
  CLC： R285.5
- Published：2012
- 稿件说明：
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[1]潘一峰,杨晓露,王建强,章丹丹.芪麝丸体外抗炎的机制[J].中国实验方剂学杂志,2012,18(18):144-147.

PAN Yi-feng1, YANG Xiao-lu2, WANG Jian-qiang1, et al. Anti-inflammatory Mechanism of Qishe Pill in vitro[J]. Chinese journal of experimental traditional medical formulae, 2012, 18(18): 144-147.
[1]潘一峰,杨晓露,王建强,章丹丹.芪麝丸体外抗炎的机制[J].中国实验方剂学杂志,2012,18(18):144-147. DOI： 10.13422/j.cnki.syfjx.2012.18.055.

PAN Yi-feng1, YANG Xiao-lu2, WANG Jian-qiang1, et al. Anti-inflammatory Mechanism of Qishe Pill in vitro[J]. Chinese journal of experimental traditional medical formulae, 2012, 18(18): 144-147. DOI： 10.13422/j.cnki.syfjx.2012.18.055.

摘要

目的:考察芪麝丸体外对小鼠RAW264.7巨噬细胞炎症模型的抗炎机制。方法:干扰素γ（1×104U.mL-1）和脂多糖（100μg.L-1）协同诱导小鼠RAW264.7巨噬细胞（1×105/mL）24 h造成炎症模型;Griess反应测定细胞上清液中一氧化氮（NO）产量;Western blot检测诱导型一氧化氮合酶（iNOS）、环氧合酶（COX-2）的蛋白表达及丝裂原活化蛋白激酶（MAPK）信号转导通路的活化情况。结果:芪麝丸（250

500

1 000 mg.L-1）呈剂量依赖性抑制细胞上清液中NO含量

且无细胞毒性。较模型组

经芪麝丸500

1 000 mg.L-1剂量处理后

iNOS蛋白表达从（1.00±0.06）下调至（0.61±0.07）和（0.02±0.15）

（P<0.01）

COX-2蛋白表达从（0.56±0.03）下调至（0.42±0.02）

（0.30±0.03）

（P<0.01）。胞外信号调节激酶（ERK）磷酸化水平从（1.04±0.04）下调至（0.79±0.06）

（0.73±0.10）

（P<0.01）。p38磷酸化水平从（0.51±0.06）下调至（0.39±0.07）

（0.29±0.15）

（P<0.05）

c-Jun氨基末端激酶（JNK）磷酸化水平从（1.05±0.03）下调至（0.65±0.02）

（0.66±0.033）

（P<0.01）。结论:芪麝丸部分通过抑制MAPK信号转导通路活化过程中关键蛋白胞外信号调节激酶（ERK）、JNK和p38丝裂原活化蛋白激酶（p38）磷酸化

下调iNOS基因和蛋白的表达从而减少NO的产量

同时下调COX-2蛋白表达

而发挥其抗炎效果。

Abstract

Objective:To study the anti-inflammatory mechanism of Qishe pill on stimulated macrophage.Method:Interferon-γ（IFN-γ） plus lipopolysaccharide（LPS） stimulated RAW 264.7 macrophage was used as inflammatory experimental model.Griess reaction for nitric oxide production and Western blot for protein expression examination were performed.Result:Qishe pill inhibited nitric oxide（NO） production in a dose-dependent manner without cytotoxicity.The protein expression of inducible nitric oxide synthase（iNOS） and cyclooxygenase（COX-2） were also suppressed by Qishe pill treatment.Furthermore

phosphorylation of extracellular signal-regulated kinase（ERK）

c-Jun NH2-terminal kinase（JNK） and p38 protein was markedly inhibited.Conclusion:Qishe pill suppressed over production of NO and iNOS expression via inhibition of phosphorylation of ERK

JNK and p38/MAPK（mitogen-activated protein kinas） activated signalling pathway partly.

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Related Author

PAN Yi-feng

YANG Xiao-lu

WANG Jian-qiang

ZHANG Dan-dan

Feng-rong ZHANG

Xiao-xuan FAN

Zhi-yong LI

Shi-huan TANG

Related Institution

Institute of Chinese Materia Medica，China Academy of Chinese Medical Sciences

College of Traditional Chinese Medicine （TCM）， Shandong University of TCM，Ji′nan

The First Clinical Medical College of Shaanxi University of Chinese Medicine

Experimental Research Center，China Academy of Chinese Medical Sciences

Beijing University of Chinese Medicine

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