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<p>Tourette syndrome (TS), predominantly affecting children and adolescents aged 2–15 years, significantly impairs quality of life and social functioning. Shaoma Zhijing granules (SMZJG), a compound traditional Chinese medicine (TCM), has demonstrated comparable efficacy to tiapride (TIA) in alleviating TS symptoms with fewer adverse effects. To elucidate its tmaterial basis and mechanism of action, we employed iminodipropionitrile (IDPN) and 2, 5-dimethoxy-4-iodoarylamine (DOI) to induce a rat model of TS. SMZJG treatment significantly ameliorated IDPN- and DOI-induced stereotyped behavioral impairments and effectively counteracted the reduction in striatum volume. Notably, SMZJG was found to markedly correct neurotransmitter imbalances, suppress M1 microglial activation, and reduce the levels of interleukin-1α (IL-1α), interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and monocyte chemoattractant protein-1 (MCP-1) in serum. These findings collectively suggest that SMZJG alleviates TS-associated behavioral disorders, potentially through mechanisms such as reducing striatal atrophy, modulating neurotransmitter imbalances, regulating abnormal neurotransmitter receptor expression, and decreasing microglial proliferation as well as levels of pro-inflammatory cytokines and chemokines in serum.</p> Graphical Abstract <p></p>

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Elucidating the material basis and therapeutic mechanisms of Shaoma Zhijing granules for tourette syndrome by UPLC/Q-TOF-MS and multiple models

  • 期刊论文

  • 发表日期：

    2025年11月25日

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  • Qian Zhao,
  • Xin-Xin Xu,
  • Jin-Na Yang,
  • Li-Juan Pei,
  • Zhou-Yi Xie,
  • Wen-Jia Wang,
  • Jing-Xuan Fu,
  • Zhao-Hui Song,
  • He Sun,
  • Kai-Jing Yan,
  • Hui Wang,
  • Yun-Hui Hu

摘要

Tourette syndrome (TS), predominantly affecting children and adolescents aged 2–15 years, significantly impairs quality of life and social functioning. Shaoma Zhijing granules (SMZJG), a compound traditional Chinese medicine (TCM), has demonstrated comparable efficacy to tiapride (TIA) in alleviating TS symptoms with fewer adverse effects. To elucidate its tmaterial basis and mechanism of action, we employed iminodipropionitrile (IDPN) and 2, 5-dimethoxy-4-iodoarylamine (DOI) to induce a rat model of TS. SMZJG treatment significantly ameliorated IDPN- and DOI-induced stereotyped behavioral impairments and effectively counteracted the reduction in striatum volume. Notably, SMZJG was found to markedly correct neurotransmitter imbalances, suppress M1 microglial activation, and reduce the levels of interleukin-1α (IL-1α), interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and monocyte chemoattractant protein-1 (MCP-1) in serum. These findings collectively suggest that SMZJG alleviates TS-associated behavioral disorders, potentially through mechanisms such as reducing striatal atrophy, modulating neurotransmitter imbalances, regulating abnormal neurotransmitter receptor expression, and decreasing microglial proliferation as well as levels of pro-inflammatory cytokines and chemokines in serum.

Graphical Abstract