Skip to main content

ORIGINAL RESEARCH article

Front. Pharmacol.
Sec. Ethnopharmacology
Volume 15 - 2024 | doi: 10.3389/fphar.2024.1447241
This article is part of the Research Topic Traditional Processing Methods in Ethnopharmacology: Enhancing Therapeutic Effects and Unveiling Mechanisms of Action View all 8 articles

DaiTongXiao improves gout nephropathy by inhibiting inflammatory response through TLR4/MyD88/NF-κB pathway

Provisionally accepted
Feifan Liu Feifan Liu Yuanmei Bai Yuanmei Bai Yan Wan Yan Wan *Shifang Luo Shifang Luo *Linao Zhang Linao Zhang *Xue Wu Xue Wu Rong Chen Rong Chen *Zili Yin Zili Yin *Yuhuan Xie Yuhuan Xie Peixin Guo Peixin Guo *
  • Yunnan University of Traditional Chinese Medicine, Kunming, China

The final, formatted version of the article will be published soon.

    Gouty nephropathy (GN) arises from factors like excessive purine intake, metabolic disorder, or abnormal synthesis, and uric acid hyper-saturation in blood, leading to urate crystals deposition in kidney tissue. Daitongxiao (DTX) is a remedy used by Dai people of China, shows efficacy in lowering uric acid levels and exhibits anti-inflammatory and kidney protective properties. A GN rat model was induced using adenine and potassium oxonate. Following DTX administration, various parameters were assessed in urine, serum, and kidney tissue. Western blot analysis evaluated TLR4/MyD88/NF-κB signaling proteins, while immunofluorescence examined NF-κB nuclear expression. DTX treatment improve kidney morphology, increased body weight and kidney index, and enhanced urinary levels of blood urea nitrogen (Bun), 24h urinary protein, uric acid (UA), and allantoin in GN rats, reducing UA, Bun, creatinine (Cre), Cystatin C (CysC), Serumamyloid A (SAA), α1-microglobulin (MG) and β2-MG in serum analysis. Renal tissue assessments showed decreased Xanthine oxidase (XOD), Hydroxyproline (Hyp), α-smooth muscle actin (α-SMA) and Collage TypeⅣ (COL-Ⅳ). Kidney damage severity was notably reduced. DTX lowered serum inflammatory factors interleukin (IL) -18, tumor necrosis factor-α (TNF-α), C-reactive protein (CRP), transforming growth factor-β1 (TGF-β1), IL-1β in rat serum, reducing chemokine Monocyte chemoattractant protein-1 (MCP-1) and adhesion factor vascular cell adhesion molecule-1(VCAM-1). Western blotting demonstrated downregulation of TLR4/MyD88/NF-κB pathway proteins, and immunofluorescence revealed reduced NF-κB expression in renal tissue. DTX exhibits significant anti-GN effects by modulating TLR4/MyD88/NF-κB pathway protein expression, reducing inflammatory factor release, and inhibiting GN progression.

    Keywords: Daitongxiao, Gout nephropathy, Traditional Chinese Medicine, TLR4/MyD88/NF-κB pathway, Mechanism research

    Received: 11 Jun 2024; Accepted: 17 Jul 2024.

    Copyright: © 2024 Liu, Bai, Wan, Luo, Zhang, Wu, Chen, Yin, Xie and Guo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Yan Wan, Yunnan University of Traditional Chinese Medicine, Kunming, China
    Shifang Luo, Yunnan University of Traditional Chinese Medicine, Kunming, China
    Linao Zhang, Yunnan University of Traditional Chinese Medicine, Kunming, China
    Rong Chen, Yunnan University of Traditional Chinese Medicine, Kunming, China
    Zili Yin, Yunnan University of Traditional Chinese Medicine, Kunming, China
    Peixin Guo, Yunnan University of Traditional Chinese Medicine, Kunming, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.