Conclusion
Obestatin exerts protective effects against ischemia injury by inhibition of astrocytes activation and decreases neuronal cell apoptosis via its antioxidant properties.
Methods
Forty-eight male Wistar rats were randomly assigned into 4 groups (sham, ischemia/reperfusion, ischemia/reperfusion+ Obestatin 1, and 5 µg/kg, n=12). Ischemia induced occlusion of both common carotid arteries for 20 min. Obestatin 1 and 5 µg/kg were injected intraperitoneally at the beginning of reperfusion period and 24 and 48 hr after reperfusion. Assessment of the antioxidant enzymes and tumor necrosis factor alpha (TNF-α) was performed by ELISA method. Caspase-3 and glial fibrillary acidic protein (GFAP) proteins expression levels were evaluated by immunohistochemical staining 7 days after ischemia.
Results
Based on the result of the current study, lower superoxide dismutase (SOD) and glutathione (GSH) (P<0.05) and higher malondialdehyde (MDA) and TNF-α levels were observed in the ischemia group than those of the sham group (P<0.01). Obestatin treatment could increase both SOD and GSH (P<0.05) and reduce MDA and TNF-α (P<0.05) versus the ischemia group. Moreover, obestatin could significantly decrease caspase-3 and GFAP positive cells in the CA1 region of hippocampus (P<0.01).