Remote limb ischemic postconditioning protects mouse brain against cerebral ischemia/reperfusion injury via upregulating expression of Nrf2, HO-1 and NQO-1 in mice

• Published in: International journal of neuroscience Vol. 126; no. 6; pp. 552 - 559
• Main Authors: Li, Pan, Su, Likai, Li, Xiaofang, Di, Weiying, Zhang, Xiangjian, Zhang, Cong, He, Tingting, Zhu, Xingyuan, Zhang, Ye, Li, Yaoru
• Format: Journal Article
• Language: English
• Published: New York Taylor & Francis 02.06.2016
• Subjects: antioxidative stress; cerebral ischemia; ischemia/reperfusion injury; neuroprotection; remote ischemic postconditioning; antioxidative stress; remote ischemic postconditioning; ischemia/reperfusion injury; cerebral ischemia; neuroprotection
• ISSN: 0020-7454; 1563-5279; 1543-5245
• DOI: 10.3109/00207454.2015.1042973

Remote ischemic postconditioning (RIPostC) is a promising therapeutic intervention, which has been discovered to reduce ischemia/reperfusion (I/R) injury in heart, kidney, brain and skeletal muscle experimentally. However, its potential protective mechanisms have not been well elucidated. The aim of this study was to investigate the protective effect of RIPostC in cerebral I/R injury and explore the new putative mechanisms of neuroprotection elicited by it. Focal cerebral ischemia was induced by transient middle cerebral artery occlusion (tMCAO) in male CD1 mice. RIPostC was generated by three cycles of 5-min reperfusion/5-min occlusion of the bilateral femoral artery on the bilateral limbs at the onset of middle cerebral artery reperfusion. RIPostC significantly improved neurological outcome, lessened infarct volume and brain edema, upregulated the expression of Nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and quinone oxidoreductase-1 (NQO-1) and activity of superoxide dismutase (SOD), and downregulaed the formation of malondialdehyde (MDA) (p < 0.05). Taken together, these findings demonstrated that RIPostC protected the brain from I/R injury after focal cerebral ischemia by reducing oxidative stress and activating the Nrf2-ARE (antioxidant response element) pathway.