بررسی ‌میزان بیان آنزیم تبدیل‌کننده‌ی TNF-a (TACE) و سطح فعالیت NF-kB در پدیده‌ی تحمل به ایسکمی‌‌ حاصل از هیپرکسی نورموباریک متناوب در مدل موش صحرایی سکته‌ی مغزی

  Background and objective: Recent studies suggest that intermittent and prolonged normobaric hyperoxia (HO) results in ischemic tolerance to reduce brain injury. In this research attempts were made to see the changes in TNF-a converting enzyme (TACE) and NF-kB activity following intermittent HO and ischemia preconditioning.   Materials and Methods: The rats were divided into two experimental groups, each consisted of 20 animals. The first group was exposed to 95% inspired HO for 4h/day for 6 consecutive days (intermittent HO InHO). The second group acting as the control, was exposed to 21% oxygen in the same chamber (normobaric normoxia or room air RA) continuously for six days (intermittent RA InRA). Each main group was subdivided to MCAO-operated (middle cerebral artery occlusion), sham-operated (without MCAO), and intact (without any surgery) subgroups. After 24hr, MCAO-operated subgroups were subjected to 60 min of right MCAO. After 24 h reperfusion, neurologic deficit score (NDS) and infarct volume were assessed in MCAO-operated subgroups. Immediately and 48 h after pretreatment, blood sampling for assessment of serum TNF- a levels were subjected. Then, the effect of intermittent HO and ischemia on NF-kB activity and TACE expression were measured.   Results: Preconditioning with intermittent HO and ischemia decreased NDS and infarct volume. Moreover InHO and MCAO-InHO upregulate TACE and increase NF-kB activity significantly.   Conclusion: Although further studies are needed to clarify the mechanisms of ischemic tolerance, InHO and ischemia seem to partly exert their effects via increase upregulation of TACE and NF-kB activity.