Ethyl pyruvate protects PC12 cells from oxygen-glucose deprivation: A potential role in ischemic cerebrovascular disease - 01/07/17
, Liping Wei a, Hongying Bai b, Yaohui Zhang a, Yuqing He aBienvenue sur EM-consulte, la référence des professionnels de santé.
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Abstract |
The protective potential of ethyl pyruvate (EP) on neuron has been investigated previously. This study was intended to investigate the effects of EP on the severity of oxygen-glucose deprivation (OGD)-induced injury in neural-like PC12 cells. PC12 cells were exposed to OGD condition with or without EP treatment. Then, cell viability, apoptosis, and the expressions of neurotrophic factors were detected. Further, Sprague–Dawley rats were intravenously administered with 5mg/kg EP for 14 days post-middle cerebral artery occlusion (MCAO). The effects of EP on the infarct volumes and neurological functions of MCAO rats were then assessed. Result showed that EP alleviated OGD-diminished cells viability, OGD-induced apoptosis, and OGD-reduced expressions of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF) and Nestin in PC-12 cells. EP blocked OGD-activated the Notch1 and nuclear factor Kappa B (NF-κB) signaling pathways in PC12 cells. Besides, in vivo data demonstrated that EP treatment decreased infarct volume and mNSS score, and increased the time spent on the rota-rod apparatus of MCAO rats. To conclude, EP protected neural-like PC12 cells from cerebral ischemia–reperfusion injury by suppressing apoptosis and promoting neural restoration. Notch1 and NF-κB pathway might implicated in the functions of EP on neuron.
Le texte complet de cet article est disponible en PDF.Abbreviations : EP, OGD, BDNF, NGF, NF-κB
Keywords : Ethyl pyruvate, Ischemic cerebrovascular disease, Oxygen-glucose deprivation, Middle cerebral artery occlusion (MCAO), Apoptosis, Notch1/NF-κB pathway
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Vol 92
P. 168-174 - août 2017 Retour au numéro
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