Details

Autor(en) / Beteiligte

• Hu, Ruiyao
• Liang, Jing
• Ding, Lan
• Zhang, Wan
• Liu, Xinjing
• Song, Bo
• Xu, Yuming

Titel

Edaravone dexborneol provides neuroprotective benefits by suppressing NLRP3 inflammasome-induced microglial pyroptosis in experimental ischemic stroke

Ist Teil von

• International immunopharmacology, 2022-12, Vol.113, p.109315-109315, Article 109315

Ort / Verlag

Elsevier B.V

Erscheinungsjahr

2022

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• •Edaravone dexborneol is a multi-target medication with both antioxidant and anti-inflammatory characteristics.•Edaravone dexborneol plays a protective role in ischemic brain injury by regulating microglia pyroptosis.•Edaravone dexborneol produces neuroprotective benefits by suppressing the NF-κB/NLRP3/GSDMD signaling pathway.•Edaravone dexborneol may have a significant role in extending the therapeutic window for acute ischemic stroke. Edaravone dexborneol (EDB) is a traditional prescription that consists of two components, edaravone and (+)-borneol, which have synergistic antioxidant and anti-inflammatory activities in animal models of ischemic stroke. Pyroptosis is a form of cell death that has only recently been discovered. In this study, we investigated the therapeutic effects and potential mechanisms of EDB in acute ischemic stroke. We used an in vivo mouse transient middle cerebral artery occlusion (tMCAO) model along with an in vitro BV2 cell oxygen-glucose deprivation (OGD) model to perform specific experiments. The executive protein of pyroptosis, gasdermin D (GSDMD), was increased after tMCAO. The administration of EDB dramatically reduced sensorimotor deficits and infarct sizes in mice with tMCAO. In addition, EDB inhibited the production of the NLRP3-inflammasome and the activation of the NF-κB signaling pathway. This effect inhibited both the in vitro and in vivo expression of inflammatory factors, including IL-1β and IL-18. Collectively, our data indicate that EDB exerted positive effects after ischemic stroke. EDB inhibited the activation of NLRP3 inflammasome-induced microglial pyroptosis in experimental ischemic stroke. The findings of this research indicate that the NF-κB/NLRP3/GSDMD signaling pathway may serve as a therapeutic target for EDB to promote functional recovery after stroke.