没食子酸调控类风湿关节炎小鼠模型的免疫应答。

Gallic acid regulates immune response in a mouse model of rheumatoid arthritis.

机构信息

Department of Laboratory, Daqing Oilfield General Hospital, Daqing, Heilongjiang, China.

Department of Rheumatism, The First Hospital of Qiqihar, Affiliated Qiqihar Hospital of Southern Medical University, Qiqihar, Heilongjiang, China.

出版信息

Immun Inflamm Dis. 2023 Feb;11(2):e782. doi: 10.1002/iid3.782.

INTRODUCTION

Previous studies revealed that gallic acid (GA) exerts anti-inflammation and immuno-regulatory properties. This study aims to explore the pharmacological activities of GA in collagen-induced arthritis (CIA) mouse model.

METHODS

Male DBA/1J mice were used to construct the CIA model. The mice were administrated with GA for 3 weeks. Clinical arthritis scores and hind paw volume were evaluated over the experimental period. qPCR and Western blot analysis were used to determine the levels of matrix metallopeptidases (MMPs) and cytokines. In addition, flow cytometry was used to measure the populations of Th17 and Treg cells. ELISAs were used to determine the cytokines in the serum and ankle joint tissues.

RESULTS

Treatment of GA (40 and 80 mg/kg/d) reduced clinical arthritis scores and hind paw volume in the CIA mouse model. Besides, treatment of GA reduced the overexpression of MMPs and modulated the dysregulation of inflammation-related cytokines. Flow cytometry showed that treatment of GA decreased the population of Th17 cells, and increased the population of Treg cells, as supported by treatment of GA regulated the Th17/Treg-related cytokines.

CONCLUSIONS

GA attenuates symptoms in the CIA mouse model by anti-inflammation and regulating Th17/Treg cell imbalance.

简介

先前的研究表明，没食子酸（GA）具有抗炎和免疫调节特性。本研究旨在探讨 GA 在胶原诱导性关节炎（CIA）小鼠模型中的药理作用。

方法

雄性 DBA/1J 小鼠用于构建 CIA 模型。用 GA 处理小鼠 3 周。在实验期间评估临床关节炎评分和后爪体积。qPCR 和 Western blot 分析用于确定基质金属蛋白酶（MMPs）和细胞因子的水平。此外，流式细胞术用于测量 Th17 和 Treg 细胞的群体。ELISA 用于测定血清和踝关节组织中的细胞因子。

结果

GA（40 和 80mg/kg/d）治疗可降低 CIA 小鼠模型中的临床关节炎评分和后爪体积。此外，GA 治疗可降低 MMPs 的过度表达，并调节炎症相关细胞因子的失调。流式细胞术显示，GA 治疗可减少 Th17 细胞的群体，并增加 Treg 细胞的群体，GA 治疗调节 Th17/Treg 相关细胞因子也支持这一结果。