Neuroprotection against focal ischemic brain injury by the peroxisome proliferator‐activated receptor‐γ agonist rosiglitazone

@article{Luo2006NeuroprotectionAF,
  title={Neuroprotection against focal ischemic brain injury by the peroxisome proliferator‐activated receptor‐$\gamma$ agonist rosiglitazone},
  author={Yumin Luo and Wei-cong Yin and Armando P. Signore and Feng Zhang and Zhen Hong and Suping Wang and Steven H. Graham and Jun Chen},
  journal={Journal of Neurochemistry},
  year={2006},
  volume={97}
}
Peroxisome proliferator‐activated receptor gamma (PPAR‐γ) is a nuclear membrane‐associated transcription factor that governs the expression of various inflammatory genes. PPAR‐γ agonists protect peripheral organs from ischemic injury. In the present study, we investigated whether the PPAR‐γ agonist rosiglitazone is neuroprotective against focal ischemic brain injury. C57/B6 mice underwent 1.5‐h middle cerebral artery occlusion, and received either vehicle or rosiglitazone treatment of 0.75, 1.5… 
The role of peroxisome proliferator-activated receptor γ, and effects of its agonist, rosiglitazone, on transient cerebral ischemic damage
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TLDR
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TLDR
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TLDR
PPAR‐γ expression, DNA binding and transcriptional activity following stroke, and rosiglitazone‐mediated protection after stroke was reversed by the PPar‐γ antagonist T0070907, suggesting that endogenous PP AR‐γ ligands may mitigate the effects of cerebral ischemia.
Neuroprotection by rosiglitazone in transient focal cerebral ischemia might not be mediated by glutamate transporter‐1#
TLDR
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The Protective Effects of Peroxisome Proliferator-Activated Receptor Gamma in Cerebral Ischemia-Reperfusion Injury
TLDR
The research progress of studies that have investigated the protective effects of PPARγ in CI/RI are summarized and the cellular and molecular mechanisms through which these effects are modulated are summarized.
Peroxisome proliferator‐activated receptorsγ (PPARγ) differently modulate the interleukin‐6 expression in the peri‐infarct cortical tissue in the acute and delayed phases of cerebral ischaemia
TLDR
It is demonstrated that cerebral PPARγ suppresses the expression of IL‐6 in ischaemic brain tissue during the initial phase of ischaemia stroke, in which the overproduction of IL-6 may aggravate neuronal damage, but not at later time points, when IL‐ 6 promotes neuroprotection and inhibits neuronal death.
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