期刊
METABOLIC BRAIN DISEASE
卷 29, 期 3, 页码 645-654出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11011-014-9548-x
关键词
Guanosine; Glutamate; Oxidative stress; Neuroprotection; Electroencephalogram; Hepatic encephalopathy
资金
- FINEP Rede Instituto Brasileiro de Neurociencia (IBN-Net) [01.06.08.42-00]
- CNPq
- CAPES
- FAPERGS
- UFRGS
- Instituto Nacional de Ciencia e Tecnologia - Neurotoxicidade e Neuroprotecao (INCT-EN)
It is well known that glutamatergic excitotoxicity and oxidative stress are implicated in the pathogenesis of hepatic encephalopathy (HE). The nucleoside guanosine exerts neuroprotective effects through the antagonism against glutamate neurotoxicity and antioxidant properties. In this study, we evaluated the neuroprotective effect of guanosine in an animal model of chronic HE. Rats underwent bile duct ligation (BDL) and 2 weeks later they were treated with i.p. injection of guanosine 7.5 mg/kg once a day for 1-week. We evaluated the effects of guanosine in HE studying several aspects: a) animal behavior using open field and Y-maze tasks; b) brain rhythm changes in electroencephalogram (EEG) recordings; c) purines and glutamate levels in the cerebral spinal fluid (CSF); and d) oxidative stress parameters in the brain. BDL rats presented increased levels of glutamate, purines and metabolites in the CSF, as well as increased oxidative damage. Guanosine was able not only to prevent these effects but also to attenuate the behavioral and EEG impairment induced by BDL. Our study shows the neuroprotective effects of systemic administration of guanosine in a rat model of HE and highlights the involvement of purinergic system in the physiopathology of this disease.
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