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Fluoxetine-enhanced autophagy ameliorates early brain injury via inhibition of NLRP3 inflammasome activation following subrachnoid hemorrhage in rats.

Jian-Ru LiHang-Zhe XuSheng NieYu-Cong PengLin-Feng FanZhi-Jiang WangCheng WuFeng YanJing-Yin ChenChi GuChun WangJing-Sen ChenLin WangChen Gao
Published in: Journal of neuroinflammation (2017)
Together, our present study indicated that NLRP3 inflammasome and caspase-1 activation play a deleterious role in early brain injury and fluoxetine mitigates NLRP3 inflammasome and caspase-1 activation through autophagy activation after SAH, providing a potential therapeutic agent for SAH treatment.
Keyphrases
  • nlrp inflammasome
  • brain injury
  • subarachnoid hemorrhage
  • cell death
  • cerebral ischemia
  • oxidative stress
  • signaling pathway
  • endoplasmic reticulum stress
  • induced apoptosis