Investigation of SREBP-1 and C/EBPβ expression during global ischemia/reperfusion-induced oxidative stress in rat brain cortex and cerebellum

Abstract

Abstract Objectives Ischemic brain injury causes neurodegeneration. This study investigated the mechanism of neurodegeneration by examining the expression of transcription factors, sterol regulatory element-binding protein-1 (SREBP-1) and CCAAT enhancer-binding protein β (C/EBPβ), in a time course. Besides oxidative stress markers such as thiobarbituric acid-reactive substances (TBARS), total thiol molecule (TTM) levels, and superoxide dismutase (SOD), glutathione-S-transferase (GST) activities were also detected. Methods In adult male rats, carotid artery occlusion and hypotension were produced for 10 min. Control groups were sham-operated. Animals were sacrificed after 24 h, 1, 2, and 4 weeks of reperfusion periods. The expression of SREBP-1 and C/EBPβ in the rat brain cortex and cerebellum was examined by Western blotting. Results C/EBPβ expression significantly increased in both cytosolic (1.19-, 1.58-fold) and nuclear (1.73-, 1.81-fold) extracts of the brain cortex after 24 h and 1 week of reperfusion. In the cerebellum, C/EBPβ expression significantly increased in 1 week, cytosolic (1.63-fold), and nuclear (1.35-fold) extracts. SREBP-1 expression significantly increased in both cytosolic (2.07-fold) and nuclear (1.41-fold) extracts of the brain cortex after 1 week of reperfusion. SREBP-1 expression significantly increased in cytosolic (2.15-fold) and nuclear (1.79-fold) extracts of cerebellum after 1 week of reperfusion. In addition, TBARS levels and SOD activities significantly increased by 43.16 % and 47.30 %, respectively, after 24 h of reperfusion. Conclusions Our findings indicate that an increase in oxidative stress parameters arose at the earlier phase of ischemic neurodegenerative processes, while SREBP-1 expression increased in the mid-phase. C/EBPβ expressions were increased at early to mid-phases of reperfusion injury.