Antioxidant and Protective Mechanisms against Hypoxia and Hypoglycaemia in Cortical Neurons in Vitro

International Journal of Molecular Sciences

José Joaquín Merino¹  César Roncero¹  Mar໚ Jesús Oset-Gasque¹  Ahmad Naddaf² 

[1] Departamento de Bioquímica y Biología Molecular II, Facultad de Farmacia, Universidad Complutense de Madrid (U.C.M.) Ciudad Universitaria, Madrid 28040, Spain; E-Mails:;Faculty of Pharmacy, Isra University, PO Box 22, Amman 11622, Jordan; E-Mail:

关键词: cortical neurons;    cerebral ischemia;    ROS formation;    antioxidant defenses;    mitochondrial membrane potential;    free radical;    SOD1/caspase-3;   

DOI  :  10.3390/ijms15022475

来源: mdpi

【 摘 要 】

In the present work, we have studied whether cell death could be induced in cortical neurons from rats subjected to different period of O₂ deprivation and low glucose (ODLG). This “in vitro” model is designed to emulate the penumbra area under ischemia. In these conditions, cortical neurons displayed loss of mitochondrial respiratory ability however, nor necrosis neither apoptosis occurred despite ROS production. The absence of cellular death could be a consequence of increased antioxidant responses such as superoxide dismutase-1 (SOD1) and GPX3. In addition, the levels of reduced glutathione were augmented and HIF-1/3α overexpressed. After long periods of ODLG (12–24 h) cortical neurons showed cellular and mitochondrial membrane alterations and did not recuperate cellular viability during reperfusion. This could mean that therapies directed toward prevention of cellular and mitochondrial membrane imbalance or cell death through mechanisms other than necrosis or apoptosis, like authophagy, may be a way to prevent ODLG damage.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland