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P2‐265: Oxidative alterations of the olfactory bulb and entorhinal cortex in early stages of Alzheimer's disease
Author(s) -
Huesa Gema,
Ferrer Isidro
Publication year - 2010
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2010.05.1315
Subject(s) - olfactory bulb , entorhinal cortex , olfaction , olfactory system , context (archaeology) , neuropathology , neuroscience , biology , astrocytosis , hippocampus , olfactory memory , alzheimer's disease , pathology , disease , central nervous system , medicine , paleontology
derivative. Results: The present study indicates that oxidative stress resulting from the treatment of H2O2 can be inhibited in the presence of our oxazine derivative, in a dose-dependent manner. Based on our findings, it seems that in this cytoprotection, inhibition of NF-kB is the main factor that protects neurons against oxidative stress induced caspase-3 activity. In addition, upregulation of HO-1 and g-GCS through Nrf2 pathway may present another possible mechanism of action of this compound. It was also found that oxazine derivative interferes the oxidation of membrane lipids, one of the primary events in oxidative cellular damage. While treatment with H2O2 increased MDA level to about 170%, compared to control, pretreatment of PC12 cells with oxazine derivative decreased MDA content to about 102%, compared to control. On the other hand, the antioxidant enzymes those serve as a detoxifying system to prevent damage caused by ROS was greatly increased in the presence of oxazine derivative. Conclusions: In summary, our results clearly indicate that our oxazine derivative prevent the H2O2-induced cell death in differentiated PC12 cells, dose-dependently. It seems that in this cytoprotection, Nrf2 and NF-kB are the main factors which protect neurons against oxidative stressinduced apoptosis.