| ARTICLES | Volume 1, Issue 7, Pages 261-266 (September 2015)

Research Article ALTERATION OF BRAIN EXPRESSION OF PROLYL ENDOPEPTIDASE IN AN ANIMAL MODEL OF HYPERAMMMONEMIA | Addaoudi Kaoutar | Hernandez-Rabaza V | Arturo García-Horsman | Vicente Felipo | Jofre Tenorio | and | Errami Mohammed |. American Journal of Innovative Research and Applied Sciences. 2015; 1(7):261-266. | PDF FULL TEXT |

ABSTRACT Baground Minimal hepatic encephalopathy (MHE) produced mild motor and cognitive disorders and predisposes to suffer hepatic encephalopathy (HE), the most severe form of the disease.  Currently, hyperammonemia (HA) and neuroinflammation are considered synergic factors involved in the pathogenesis of MHE and HE. The serine peptidase prolyl endopeptidase (PREP) cleaves short peptides (<30 amino acids) at the C-side of a proline residue. It has been proposes that PREP may play a role in the inflammatory response through peptide modulation. Objectives: In this paper we showed our results in relation to the expression of PREP in a model of MHE produces by induction of chronic moderate HA. Methods: Brain samples were collected from HA rats and PREP expression was determined by immunohistochemistry analysis and immunoblotting assessment in the neocortex, hippocampus, striatum and cerebellum. Results: The results indicated that HA produces PREP expression alterations in most of the areas analyzed. After 8 weeks of HA the expression of PREP was increased in the motor cortex, CA1 region of the hippocampus, the caudate putamen of the striatum and in the cerebellum. Conclusions: these results may indicate that prep increase may have a role in alterations seen in hyperammonemia without liver impairment. Key words: Minimal hepatic encephalopathy, ammonium.