INVESTIGADORES
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congresos y reuniones científicas
Título:
Hippocampal apoptosis in a low-grade hepatic encephalopathy model.
Autor/es:
PERAZZO, J.C.; LORES-ARNAIZ, S.; ROSELLÓ, D.M.; CZERNICZYNIEC, A.; LAGO, N.; TALLIS, S.; LEMBERG, A. ; BUSTAMANTE, J.
Lugar:
Abano Terme
Reunión:
Congreso; 13th International Symposium on Hepatic Encephalopathy and Nitrogen Metabolism.; 2008
Resumen:
In previous reports we described
mitochondrial hippocampal (H) morpho-functional alterations in blood brain
barrier in rats with portal vein ligature (PVL). PVL induced portal hypertension,
moderate hyperammonemia and is a valid model to study low-grade hepatic
encephalopathy (lgHE). The aim of this work was to study early alterations in H
in PVL rats.
Male Wistar rats weighing 250 g were
divided into two groups: Group I, (n=12) with PVL and Group II, (n=12) was
sham-operated. Ten days after PVL, portal pressure was recorded and plasma
ammonia was determined. After that, hippocampal
brains from both groups were dissected. To
determine de presence of apoptosis the DNA
decreases fragmentation method,
TUNEL, was used. Isolation of mitochondrial fraction
further mitochondrial purification for Western blot analysis was performed.
Sub-mitochondrial membranes were obtained from mitochondria by twice freezing,
thawing and homogenizing the suspension. Western blotting and chemiluminescence from H for Bax
mitochondrial association was determined in mitochondrial purified fractions
and mtNOS. Mitochondrial membrane
potential in the hippocampus (cytometric, probe DIOC6) and release of cytochrome c was registered. Results: TUNEL
determination was positive in CA4 and CA1 H areas, Bax expression and release
of cytochrome c was significantly higher in HP group and mtNOS expression and
activity were significantly lower in HP. Extensive decrease in mitochondrial
membrane potential was seen. Quantification of this process showed 30% depolarization in
Group I when compared with Group II.
Conclusions: Early changes in H area in low-grade hepatic encephalopathy
could be due to apoptosis triggered by the intrinsic mitochondrial pathway.