Research on Mechanism of Guizhi Shaoyao Zhimu Tang in Treatment of Gouty Arthritis Based on Toll-MyD88 Signaling Pathway

WANG Yong-hui; FANG Shu-biao; LI Yan-yan; ZHOU Ran

doi:10.13422/j.cnki.syfjx.2016210121

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Research on Mechanism of Guizhi Shaoyao Zhimu Tang in Treatment of Gouty Arthritis Based on Toll-MyD88 Signaling Pathway

更新时间：2024-01-04

- Research on Mechanism of Guizhi Shaoyao Zhimu Tang in Treatment of Gouty Arthritis Based on Toll-MyD88 Signaling Pathway
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 22, Issue 21, Pages: 121-126(2016)
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.2016210121
  CLC： R285.5
- Published：2016
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WANG Yong-hui, FANG Shu-biao, LI Yan-yan, et al. Research on Mechanism of Guizhi Shaoyao Zhimu Tang in Treatment of Gouty Arthritis Based on Toll-MyD88 Signaling Pathway[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(21): 121-126.
DOI：

WANG Yong-hui, FANG Shu-biao, LI Yan-yan, et al. Research on Mechanism of Guizhi Shaoyao Zhimu Tang in Treatment of Gouty Arthritis Based on Toll-MyD88 Signaling Pathway[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(21): 121-126. DOI： 10.13422/j.cnki.syfjx.2016210121.

摘要

目的：观察桂枝芍药知母汤（GD）对尿酸钠致痛风性关节炎（GA）模型大鼠关节滑膜组织中Toll-髓性分化因子88（MyD88）信号通路炎性信号表达的影响，探讨其相关的作用机制。方法： 180只雄性SD大鼠随机分配到3个实验，分别为关节滑膜免疫组织化学技术（IHC）实验、酶联免疫吸附测定（ELISA）实验、蛋白质免疫印迹（Western blot）实验。各实验取大鼠60只，按体重随机分为6组，每组10只，分别为模型组，正常组，GD高、中、低剂量组（4，8，16 g·kg-1），秋水仙碱阳性药组（3×10-4 g·kg-1）。实验组均ig给药，正常组、模型组给予等容积的蒸馏水，每天1次，连续给药7 d。第5天ig前，大鼠足踝关节注射尿酸钠悬液诱导GA。取大鼠关节滑膜组织，IHC检测受体Toll样受体-2（Toll-like receptor 2，TLR-2），TLR-4的表达，Image-Pro Plus 6.0图像分析系统测定平均积分吸光度IA，ELISA测定环氧化酶-2（cyclooxygenase-2，COX-2），转化生长因子-β1（transforming growth factor-β1，TGF-β1）表达，Western blot检测MyD88，核因子κB酶抑制剂-β（inhibitor κB kinaseβ，IκK-β），核因子κB抑制蛋白α（NF-κB inhibitor α，IκB-α），过氧化物酶体增殖物激活受体-γ（peroxisome proliferator-activated receptor-γ，PPAR-γ）表达水平。结果：造模72 h后，与正常组比较，GA模型大鼠关节滑膜组织中TLR-2，TLR-4平均IA，MyD88，IκK-β蛋白及COX-2表达水平明显增高（P<0.05）；与模型组比较，GD中、高剂量组TLR-2，TLR-4平均IA，MyD88，IκK-β蛋白及COX-2含量表达均明显低于模型组（P<0.05）；而TGF-β1含量及IκB-α，PPAR-γ蛋白表达水平明显增高（P<0.05）；GD各剂量组IκK-β蛋白无明显变化。结论： GD治疗GA的作用机制可能与降低TLR-2，TLR-4受体及MyD88蛋白表达，增加PPAR-γ，IκB-α表达，抑制NF-κB活化，降低Toll-MyD88信号通路炎性因子表达有关。

Abstract

Objective: To investigate the effect of Guizhi Shaoyao Zhimu Tang (GT) on inflammatory signal expression of Toll-MyD88 in synovial tissues of joint of rats with monosodium urate crystal-induced gouty arthritis (GA). Method: Totally 180 male SD rats were randomly divided into 3 experiments

namely IHC

ELISA and Western blot experiments

with 60 rats in each experiment. In each experiment

60 rats were included and divided into 6 groups

namely model group

normal group

high

medium and low-dose GD group (4

16 mg·kg-1) and colchicine group (3×10-4 g·kg-1)

with 10 rats in each group according to weight. All of experimental groups were treated with medicine through gastric administration

normal and model groups were given equal volume of distilled water. Medicine or distilled water was given once daily for consecutively seven days throughout the experiments. On the fifth day

GA model was induced through injection with monosodium urate in the ankle joint cavity of rats. The synovial tissues of the rats were taken

expressions of Toll like receptor-2

4 in synovial tissues of the joint of rats were detected with immunohistochemistry

IA was measured with Image-Pro Plus 6.0 analysis system. ELISA was used to determine expressions of cyclooxygenase-2 (COX-2) and transforming growth factor-β1 (TGF-β1).The expression levels of Myeloid differentiation factor-88 (MyD88)

nuclear factor enzyme inhibitor (IκK-β)

nuclear factor κB inhibitory protein (IκB-α) and peroxisome proliferator-activated receptor gamma (PPAR-γ) were detected by Western blot. Result: Compared with normal group after 72 hours

average IA of TLR-2

TLR-4 and the expression level of MyD88

IκK-β

COX-2 in synovial tissues of the GA rats significantly increased; compared with normal group

average IA of TLR-2

TLR-4 and the expression level of MyD88

IκK-β

COX-2 significantly decreased in medium and high-dose GT groups (P<0.05)

whereas TGF-β1

IκB-α and PPAR-γ protein expressions significantly increased (P<0.05)

with no significant change in IκK-β in all GT groups. Conclusion: The action mechanism of GT on gouty arthritis in rats may be related to decreases in the expression levels of TLR-2

TLR-4 and MyD88 protein expressions

and increases in the expression of PPAR-γ and IκB-α

and inhibition of the activation of NF-κB

and reduction of the expression of inflammatory factors in Toll-MyD88 signaling pathway.

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Related Institution

Institute of Chinese Medicine，Heilongjiang University of Chinese Medicine

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