Anti-inflammatory Mechanism of Qishe Pill

PAN Yi-feng; YANG Xiao-lu; WANG Jian-qiang; ZHANG Dan-dan

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Anti-inflammatory Mechanism of Qishe Pill

更新时间：2024-09-23

- Anti-inflammatory Mechanism of Qishe Pill
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 18, Issue 18, Pages: 144-147(2012)
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- Published：2012
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PAN Yi-feng, YANG Xiao-lu, WANG Jian-qiang, et al. Anti-inflammatory Mechanism of Qishe Pill [J]. Chinese journal of experimental traditional medical formulae, 2012, 18(18): 144-147.
DOI：

PAN Yi-feng, YANG Xiao-lu, WANG Jian-qiang, et al. Anti-inflammatory Mechanism of Qishe Pill [J]. Chinese journal of experimental traditional medical formulae, 2012, 18(18): 144-147. DOI：

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(1×104 U ·mL-1)和脂多糖(100 μg ·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-feng1

YANG Xiao-lu2

WANG Jian-qiang1

ZHANG Dan-dan2

Feng-rong ZHANG

Xiao-xuan FAN

Zhi-yong LI

Shi-huan TANG

Related Institution

Shanghai SUNDISE Chinese Medicine Co.Ltd.

Murad Research Institute for Modernized Chinese Medicine,Shanghai University of Traditional Chinese Medicine

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

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