The Effect of Preconditioning with Prolonged and Intermittent Normobaric ?Hyperoxia on Upregulating TNF-? Converting Enzyme and Increasing Serum ?TNF-? Level in Male Rats
Trauma Monthly: 12 (3); 197-208 Article Type: Research Article
January 1, 2007
January 1, 2007
A. The Effect of Preconditioning with Prolonged and Intermittent Normobaric ?Hyperoxia on Upregulating TNF-? Converting Enzyme and Increasing Serum ?TNF-? Level in Male Rats,
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Introduction: Ischemic preconditioning (IPC) is an endogenous phenomenon that can induce ischemic tolerance (IT) in a variety of organs such as brain. Noxious stimuli applied at close to but below the threshold of cell injury induce adaptive responses that protect the brain against additional stress from the same (tolerance) or other (cross-tolerance) stimuli. In this study, we examined the effect of intermittent and prolonged doses of normobaric hyperoxia (NBHO) on neurologic deficit scores, serum TNF-α level, and gene expression of TNF-α converting enzyme (TACE). Material and Method: The rats were exposed to NBHO in prolonged (24h) and intermittent (every 4 hours for 6 days) groups. Each group subdivided into three subgroups. After 24 hours, the first subgroup underwent MCAO for 60 minutes followed by 24h of reperfusion. Then, IT induced by intermittent and prolonged NBHO were measured by neurologic deficit scores. The second and third subgroups, called sham-operated and intact subgroups respectively, were considered for the assessment of the effect of NBHO on serum TNF-α level and gene expression of TNF-α converting enzyme. Result: Our findings indicated that intermittent and prolonged NBHO were involved in the induction of IT. Pretreatment with prolonged and intermittent NBHO reduced neurologic deficit scores significantly. Prolonged and intermittent NBHO increased serum TNF-α level and gene expression of TNF-α converting enzyme with the effect of prolonged NBHO being significantly stronger. Also, intermittent NBHO with ischemia significantly increased serum TNF-α level and gene expression of TNF-α converting enzyme rather than intermittent NBHO alone . Conclusion: Although further studies are needed to clarify the mechanisms of ischemic tolerance, intermittent and prolonged NBHO seem to partly exert their effects via increasing serum TNF-α levels and upregulation of TNF-α converting enzyme.
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