Jianpi Qingre Tongluo Prescription (Huangqin Qingrechubi Capsule) alleviates inflammation and hypercoagulability by inhibiting the JAK2/STAT3 pathway via CircRNA 104633 downregulation in gouty arthritis

IF 5.4 2区医学 Q1 CHEMISTRY, MEDICINAL Journal of ethnopharmacology Pub Date : 2025-02-25 DOI:10.1016/j.jep.2025.119552

Xianheng Zhang , Qi Han , Jian Liu , Yiming Chen , Xiang Ding , Xiaolu Chen

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Abstract

Ethnopharmacological relevance

Gouty arthritis (GA) is characterized by intermittent inflammatory pain, which dramatically compromises the quality of life of patients. Huangqin Qingrechubi Capsule (HQC) is an empirical traditional Chinese medicine prescription used to treat GA for over 20 years, with favorable efficacy. However, little is known about the specific mechanism of action of HQC in GA treatment.

Purpose

This study probed the mechanism of action of HQC in the treatment of GA from anti-inflammatory and anticoagulation aspects.

Methods

Initially, a retrospective clinical analysis was performed to observe the effects of HQC on inflammatory and coagulation indexes in GA patients. Subsequently, the expression of CircRNA 104633 and inflammatory and coagulation factors was detected in peripheral blood mononuclear cells (PBMCs) harvested from recruited GA patients before and after HQC treatment, followed by the analysis of the correlation between CircRNA 104633 and other indexes. The anti-inflammatory and anticoagulation mechanisms of HQC in GA treatment via CircRNA 104633 were further investigated through a co-culture model composed of GA-PBMCs and fibroblast-like synoviocytes (FLSs). Finally, a rat model of monosodium urate-induced GA was established for in vivo verification.

Results

HQC reduced the levels of HCRP, ESR, and D-D in GA patients. In the PBMCs of GA patients, HQC decreased CircRNA 104633 expression, and CircRNA 104633 expression was closely related to inflammatory and coagulation indexes. CircRNA 104633 upregulation fostered inflammation and hypercoagulability in GA by activating the JAK2/STAT3 pathway, whilst HQC reversed the imbalance of inflammatory and coagulation factors by downregulating CircRNA 104633. Furthermore, HQC played anti-inflammatory and anticoagulant roles in GA rats by blocking the JAK2/STAT3 pathway.

Conclusion

HQC protects against inflammation and hypercoagulability in GA by inhibiting CircRNA 104633 and the JAK2/STAT3 pathway, which supports the development of therapeutic targets and drugs for GA.

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健脾清热通络方（黄芩清热解痹胶囊）通过抑制痛风性关节炎中CircRNA 104633下调JAK2/STAT3通路，减轻炎症和高凝性

风湿性关节炎（GA）的特点是间歇性炎症性疼痛，严重影响患者的生活质量。黄芩清热解痹胶囊（HQC）是治疗GA已有20多年历史的经验中药方剂，疗效良好。然而，HQC在GA治疗中的具体作用机制尚不清楚。目的从抗炎、抗凝两方面探讨HQC治疗GA的作用机制。方法通过回顾性临床分析，观察HQC对GA患者炎症及凝血指标的影响。随后，在招募的GA患者HQC治疗前后采集的外周血单个核细胞（PBMCs）中检测CircRNA 104633和炎症、凝血因子的表达，并分析CircRNA 104633与其他指标的相关性。通过GA- pbmcs和成纤维细胞样滑膜细胞（FLSs）组成的共培养模型，进一步研究了HQC在通过CircRNA 104633治疗GA中的抗炎和抗凝机制。最后，建立尿酸钠诱导的GA大鼠模型进行体内验证。结果shqc降低了GA患者的HCRP、ESR和D-D水平。在GA患者的PBMCs中，HQC降低了CircRNA 104633的表达，CircRNA 104633的表达与炎症和凝血指标密切相关。CircRNA 104633的上调通过激活JAK2/STAT3通路促进GA的炎症和高凝性，而HQC通过下调CircRNA 104633逆转炎症和凝血因子的失衡。此外，HQC通过阻断JAK2/STAT3通路在GA大鼠中发挥抗炎和抗凝作用。结论hqc通过抑制CircRNA 104633和JAK2/STAT3通路抑制GA的炎症和高凝性，为GA治疗靶点和药物的开发提供支持。

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来源期刊

Journal of ethnopharmacology 医学-全科医学与补充医学

CiteScore

10.30

自引率

5.60%

发文量

967

审稿时长

77 days

期刊介绍： The Journal of Ethnopharmacology is dedicated to the exchange of information and understandings about people''s use of plants, fungi, animals, microorganisms and minerals and their biological and pharmacological effects based on the principles established through international conventions. Early people confronted with illness and disease, discovered a wealth of useful therapeutic agents in the plant and animal kingdoms. The empirical knowledge of these medicinal substances and their toxic potential was passed on by oral tradition and sometimes recorded in herbals and other texts on materia medica. Many valuable drugs of today (e.g., atropine, ephedrine, tubocurarine, digoxin, reserpine) came into use through the study of indigenous remedies. Chemists continue to use plant-derived drugs (e.g., morphine, taxol, physostigmine, quinidine, emetine) as prototypes in their attempts to develop more effective and less toxic medicinals.