Research Progress of the Mechanism of Endogenous Antioxidant Stress in Cerebral Ischemic Preconditioning and Ischemia Reperfusion Injury

doi:10.3969/j.issn.2095-1396.2016.02.008

Abstract

Abstract: Cerebral ischemic preconditioning （CIP） induced by sublethal transient cerebral ischemia could increase the tolerance of the brain tissue to subsequent lethal ischemia by activating the endogenous protective factor or signaling pathways. Establishing such a tolerance involved multiple mechanisms：resistance to apoptosis，antioxidant stress，inhibiting the inflammatory response，adjusting the excitatory and inhibitory neurotransmitter，vascular remodeling，protecting blood brain barrier，maintaining energy metabolism and mitochondrial membrane potential and activating the DNA repair and self-repair etc. However，oxidative stress damaging，free radical chain reacting is the core of ischemia-reperfusion injury. Therefore，a better understanding of the mechanism of cerebral ischemic preconditioning and endogenous antioxidant stress in the ischemia reperfusion injury could provide theoretical basis for clinical treatment of ischemia anoxic encephalopathy.

Key words: cerebral ischemic preconditioning, ischemia reperfusion injury, endogenous antioxidant stress, signaling pathways

CLC Number:

R964

WANG Huan-huan, XUE Qian, ZOU Yu-an. Research Progress of the Mechanism of Endogenous Antioxidant Stress in Cerebral Ischemic Preconditioning and Ischemia Reperfusion Injury[J]. ACTA NEUROPHARMACOLOGICA, 2016, 6(2): 46-52.

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