An investigation into the EGF and TNF-α levels and the thioredoxin system in rats exposed to cerebral ischemia

Cerebral ischemia induces the consumption of the energy substrates and the inflammatory alterations, and the increases the intracellular calcium. Depending on the duration and the intensity of ischemia, endoneuronal edema, demyelination, depolarization of synaptic membranes and neuronal degeneration are produced. In this study, TrxR activity, EGF and TNF-? in cerebral ischemic, periischemic normal and sham operated rat brains were investigated. Furthermore, it was aimed to compare the paralel effects in Trx system and EGF function, as well as adverse effects of TNF-? in prolonged ischemia. Brain tissue TrxR activity in ischemic region of one group (48th h ischemia) decreased significantly compared with the control group. However there was a statistically significant increase at 96th h ischemia compared to 48th h ischemia. The EGF levels of ischemic brain tissue increased significantly in a group (96th h ischemia) in comparison with the control group. There was no statistical significancy in the TNF-? levels between the ischemic groups and the control group, but there was a statistically significant increase at 96th h ischemia compared to 48th h ischemia. In conclusion; present study showed that TrxR activity decreased in ischemia-induced oxidative stress. EGF levels increased significantly whereas TNF-? levels did not change in ischemic brain regions as compared to the control group. As a result it could be said that, TrxR activity was reduced by oxidative stress. On the other hand EGF levels increased to exhibit neurotrophic and neuroprotective effects.