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<p>Neuroinflammation, particularly through the NLRP3 inflammasome, plays a significant role in the progression of Parkinson's disease (PD). Icaritin (ICT), a flavonoid compound derived from Epimedium, has demonstrated potential therapeutic effects on PD. In this study, an MPTP-induced PD mouse model was used to evaluate the impact of ICT. The mice were treated with ICT through intragastric administration, and their motor functions were assessed by the rotarod test and the pole test. Immunofluorescence was used to examine the expression of TH, Iba1, and GFAP, and Western blotting was used to measure changes in the levels of NLRP3 and other relevant proteins. The results showed that ICT significantly improved motor dysfunction induced by MPTP, reduced dopaminergic neuronal damage, diminished glial cell activation, and inhibited the expression of proteins in the NLRP3 signalling pathway. These findings suggest that ICT has a protective effect on the MPTP-induced PD mouse model and that its mechanism of action is likely related to the inhibition of NLRP3-mediated neuroinflammation.</p> Graphical Abstract <p></p>

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Icaritin ameliorates MPTP-induced Parkinson's disease model by targeting the NLRP3 inflammasome pathway

  • 期刊论文

  • 发表日期：

    2026年3月7日

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  • Chengnian Yang,
  • Yuanyuan Li,
  • Tingting Liu,
  • Rui Liang,
  • Juan Huang,
  • Yong Luo,
  • Nanqu Huang

摘要

Neuroinflammation, particularly through the NLRP3 inflammasome, plays a significant role in the progression of Parkinson's disease (PD). Icaritin (ICT), a flavonoid compound derived from Epimedium, has demonstrated potential therapeutic effects on PD. In this study, an MPTP-induced PD mouse model was used to evaluate the impact of ICT. The mice were treated with ICT through intragastric administration, and their motor functions were assessed by the rotarod test and the pole test. Immunofluorescence was used to examine the expression of TH, Iba1, and GFAP, and Western blotting was used to measure changes in the levels of NLRP3 and other relevant proteins. The results showed that ICT significantly improved motor dysfunction induced by MPTP, reduced dopaminergic neuronal damage, diminished glial cell activation, and inhibited the expression of proteins in the NLRP3 signalling pathway. These findings suggest that ICT has a protective effect on the MPTP-induced PD mouse model and that its mechanism of action is likely related to the inhibition of NLRP3-mediated neuroinflammation.

Graphical Abstract