engleski

Hyperbaric oxygen treatment: the influence on the superoxide dismutase activity and JNK activation in the optic nerves of rats exposed to global cerebral ischemia

Introduction: Cerebral ischemia is determined with several different toxic processes including excitotoxicity, metabolic toxicity and oxidative stress. Because loss of oxygen initiates a variety of intracellular and metabolic changes in cerebral ischemia, an increase in the oxygen delivery to the cerebral tissue might prevent neuronal damage and ameliorate brain recovery after ischemia. Hyperbaric oxygen (HBO) treatment has been considered as a method to improve tissue oxygen delivery. Although the effectiveness of HBO treatment has been controversial for many years, the results presented in some experimental models of cerebral ischemia, such as in a few clinical reports, have been promising. However, the biochemical and molecular mechanisms of such treatment in cerebral ischemia are not extensively studied. The objectives of our study was to determine: a) the influence of global cerebral ischemia on the superoxide dismutase (SOD) activity and JNK activation in the optic nerves at different time points after ischemia and b) to evaluate the effect of HBO treatment after cerebral ischemia on the mentioned parameters. Materials and Methods: Hannover-Wistar rats were exposed to global cerebral ischemia of 20-min duration (Pulsinelli and Brierly, 1979) and were either sacrificed or exposed to the first HBO treatment 2, 24, 48 or 168 h after ischemic procedure (for SOD activity measurements) or 5 and 10 min, 1, 6 and 12 h after ischemia (for determinations of JNK activation). HBO treatment (2 ATA ; 98.5 % oxygen) was repeated for seven consecutive days, once per day. Each treatment lasted for 60 min. Results: The results of the presented experiments demonstrated a statistically significant increase in the SOD activity after 24, 48 and 168 h of reperfusion in the optic nerves of non HBO-treated ischemic animals, as well as in the ischemic animals treated with HBO. The JNK activation in the optic nerves of the ischemic animals was registered after all reperfusion periods tested. Maximal activation was found 1 h after ischemia but second strong activation signal was detected again at 12 h of reperfusion period. HBO treatment decreased the intensity of JNK activation signals during all reperfusion periods tested. Conclusion: Our results indicate that global cerebral ischemia induced a significant increase in SOD activity and that the level of SOD activity in ischemic animals was not changed after HBO administration. Activation of JNK was implicated in early and later periods of reperfusion injury. HBO treatment decreased the level of JNK activation, indicated its possible beneficial role in the treatment of global brain ischemia.

hyperbaric oxygen treatment; global cerebral ischemia; superoxide dismutase; JNK; optic nerves; rat

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