Normobaric hyperoxia induces ischemic tolerance and upregulation of glutamate transporters in the rat brain and serum TNF-alpha level |
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| Authors: | Bigdeli Mohammad Reza Hajizadeh Sohrab Froozandeh Mehdi Heidarianpour Ali Rasoulian Bahram Asgari Ali Reza Pourkhalili Khalil Khoshbaten Ali |
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| Affiliation: | aFaculty of Biological Sciences, Shahid Beheshti University, G.C., Tehran, Iran;bDepartment of Physiology, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran;cDepartment of Medical Biotechnology, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran;dDepartment of Physical Education and Sport Sciences, Bu-Ali Sina University, Hamadan, Iran;eRazi Herbal Medicines Research Center, Lorestan University (Medical Sciences), Khoramabad, Iran;fResearch Center for Chemical Injuries, Baqiyatallah Medical Sciences University, Tehran, Iran |
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| Abstract: | Recent studies suggest that intermittent and prolonged normobaric hyperoxia (HO) results in ischemic tolerance to reduce ischemic brain injury. In this research, we attempted to see changes in excitatory amino acid transporters (EAATs) and TNF-α levels following prolonged and intermittent hyperoxia preconditioning. Rats were divided into four experimental groups, each of 21 animals. The first two were exposed to 95% inspired HO for 4 h/day for 6 consecutive days (intermittent HO, InHO) or for 24 continuous hours (prolonged HO, PrHO). The second two groups acted as controls, and were exposed to 21% oxygen in the same chamber. Each main group was subdivided to middle cerebral artery occlusion (MCAO-operated), sham-operated (without MCAO), and intact (without any surgery) subgroups. After 24 h from pretreatment, MCAO-operated subgroups were subjected to 60 min of right MCAO. After 24 h reperfusion, neurologic deficit score (NDS) and infarct volume were measured in MCAO-operated subgroups. EAATs expression and serum TNF-α levels were assessed in sham-operated and intact subgroups. Preconditioning with prolonged and intermittent HO decreased NDS and upregulated EAAT1, EAAT2, and EAAT3 and increased serum TNF-α levels significantly. Although further studies are needed to clarify the mechanisms of ischemic tolerance, the intermittent and prolonged HO seems to partly exert their effects via increase serum TNF-α levels and upregulation of EAATs. |
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| Keywords: | Normobaric hyperoxia Brain ischemia tolerance Stroke Neuroprotection Glutamate transporter TNF-α Excitatory amino acid transporter Ischemic preconditioning MCAO |
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