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Snap25 attenuates neuronal injury via reducing ferroptosis in acute ischemic stroke.
Si, Wenwen; Sun, Bin; Luo, Jing; Li, Zhen; Dou, Yuhong; Wang, Qizhang.
Afiliación
  • Si W; Traditional Chinese Medicine Innovation Research Center, Shenzhen Hospital of Integrated Traditional Chinese and Western Medicine, Shenzhen, Guangdong 518104, PR China. Electronic address: siwenwen2008@163.com.
  • Sun B; School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei, Anhui 230012, PR China.
  • Luo J; School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei, Anhui 230012, PR China.
  • Li Z; Traditional Chinese Medicine Innovation Research Center, Shenzhen Hospital of Integrated Traditional Chinese and Western Medicine, Shenzhen, Guangdong 518104, PR China.
  • Dou Y; Traditional Chinese Medicine Innovation Research Center, Shenzhen Hospital of Integrated Traditional Chinese and Western Medicine, Shenzhen, Guangdong 518104, PR China.
  • Wang Q; Department of Neurology, Shenzhen Hospital of Integrated Traditional Chinese and Western Medicine, Shenzhen, Guangdong 518104, PR China. Electronic address: qizhangwang2023@163.com.
Exp Neurol ; 367: 114476, 2023 09.
Article en En | MEDLINE | ID: mdl-37393984
Due to the limited clinical treatment options for acute ischemic stroke (AIS), there is still an urgent requirement for in-depth research on the pathogenesis of AIS and the development of efficient therapeutic approaches and agents. Literature reports reveal that ferroptosis may play an important role in the pathogenesis of AIS. However, the specific mechanism and the molecular target of action of ferroptosis in AIS injury remains unclear. In this study, we constructed AIS rat and PC12 cell models. We applied RNAi-mediated knockdown and gene overexpression technologies to investigate whether Snap25 (Synaptosome-associated protein 25 kDa) can regulate the level of AIS damage by interfering with the level of ferroptosis in AIS. The in vivo and in vitro results revealed that the level of ferroptosis significantly increased in the AIS model. Snap25 gene overexpression significantly inhibited the ferroptosis level and decreased the AIS damage and OGD/R injury level in the model group. Snap25 silencing exacerbated the ferroptosis level and aggravated OGD/R injury in PC12 cells. The overexpression and silencing of Snap25 can significantly affect the expression level of ROS, suggesting that the regulatory effect on the ROS level may be an important factor in regulating ferroptosis in AIS by Snap25. In conclusion, the findings of this study suggested that Snap25 has a protective effect against ischemia/reperfusion injury by reducing ROS levels and ferroptosis levels. This study further confirmed the involvement of ferroptosis in the process of AIS injury and explored the regulatory mechanism of Snap25 on the ferroptosis level in AIS, which could provide a promising therapeutic target for ischemic stroke treatment.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Daño por Reperfusión / Accidente Cerebrovascular / Ferroptosis / Accidente Cerebrovascular Isquémico Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Exp Neurol Año: 2023 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Daño por Reperfusión / Accidente Cerebrovascular / Ferroptosis / Accidente Cerebrovascular Isquémico Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Exp Neurol Año: 2023 Tipo del documento: Article Pais de publicación: Estados Unidos