<p>Both clinical and preclinical evidence showed that electroacupuncture (EA) at Baihui (Governing Vessel 20, GV20) and Dazhui (GV14) could relieve sensorimotor disability after ischemic stroke (IS). However, the mechanism behind this therapeutic remains to be unraveled, and the current findings of its underlying mechanism are mainly focusing on neurons, with little evidence from astrocyte. Astrocyte plays an essential role in IS pathology, and IL-17A as a critical mediator in IS. This study aimed to investigate the relationship between the activity of astrocyte and expression of IL-17A during the regulation of sensorimotor function. The sensorimotor-related behaviors in mice were assessed by using Adhesive removal test and Rotarod test, and the expression/function of IL-17A was evaluated by ELISA, RT-PCR, and Western Blot. In vivo calcium activity of astrocyte was detected by two-photon calcium imaging. Our results revealed that EA preconditioning promoted the recovery of sensorimotor function in IS mice, and this therapeutic effect was absent when the astrocytic activity was chemogenetically inhibited. In addition, astrocytic calcium activity of IS mice could be mimicked by overexpressing IL-17A. Altogether, these results suggested the IL-17A in the astrocyte may play a key role in the functional recovery after stroke. These findings not only elucidate a critical pathway for understanding how IL-17A in astrocytic calcium activity influences the functional recovery after stroke, but also suggest a potential valuable therapeutic strategy for stroke.</p> Graphical Abstract <p></p>

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The IL-17A modulating astrocytic activity was associated with the electroacupuncture-mediated improvement of sensorimotor ability after stroke

  • Yuenming Yau,
  • Zeli Li,
  • Zhiyuan Jiang,
  • Jianyu Luo,
  • Zhennan Wu,
  • Chang Liu,
  • Nenggui Xu,
  • Lulu Yao

摘要

Both clinical and preclinical evidence showed that electroacupuncture (EA) at Baihui (Governing Vessel 20, GV20) and Dazhui (GV14) could relieve sensorimotor disability after ischemic stroke (IS). However, the mechanism behind this therapeutic remains to be unraveled, and the current findings of its underlying mechanism are mainly focusing on neurons, with little evidence from astrocyte. Astrocyte plays an essential role in IS pathology, and IL-17A as a critical mediator in IS. This study aimed to investigate the relationship between the activity of astrocyte and expression of IL-17A during the regulation of sensorimotor function. The sensorimotor-related behaviors in mice were assessed by using Adhesive removal test and Rotarod test, and the expression/function of IL-17A was evaluated by ELISA, RT-PCR, and Western Blot. In vivo calcium activity of astrocyte was detected by two-photon calcium imaging. Our results revealed that EA preconditioning promoted the recovery of sensorimotor function in IS mice, and this therapeutic effect was absent when the astrocytic activity was chemogenetically inhibited. In addition, astrocytic calcium activity of IS mice could be mimicked by overexpressing IL-17A. Altogether, these results suggested the IL-17A in the astrocyte may play a key role in the functional recovery after stroke. These findings not only elucidate a critical pathway for understanding how IL-17A in astrocytic calcium activity influences the functional recovery after stroke, but also suggest a potential valuable therapeutic strategy for stroke.

Graphical Abstract