Author/Authors :
SAEEDI BORUJENI، Mohammad Javad نويسنده Department of Anatomy and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran , , Hami، Javad نويسنده Department of Anatomical sciences, School of Medicine, Birjand University of Medical Sciences, Birjand, Iran , , Haghir، Hossein نويسنده , , Rastin، Maryam نويسنده Immunology Research Center, Department of Immunology and Allergy, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran , , SAZEGAR، Ghasem نويسنده Department of Anatomy and Cell Biology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran ,
Abstract :
Objective
Simple Febrile Seizure (SFS) is the most common seizure disorder in
childhood, and is frequently described as inoffensive disorder. Nevertheless,
there is evidence suggesting the association between neonatal febrile seizures
and hippocampal abnormalities in adulthood. This study was conducted at
evaluating the hippocampal expression of pro-apoptotic Bax and anti-apoptotic
Bcl-2 proteins following SFS induction in rat neonates.
Materials & Methods
Febrile seizure was modeled by hyperthermia-induced seizure in 22-dayold
male rats by a hot water bath. The animals were divided into two groups
based on the presence or absence of seizure behaviors: Hyperthermia without
seizure (n=10) and hyperthermia with seizure (n=10). To control the effects of
environmental stress a sham-control group was also added (n=10). The rats’
hippocampi were dissected 2 or 15 days after hyperthermia. The expression
of Bax and Bcl-2 proteins were measured using Western Blotting technique.
Results
The hippocampal expression of Bcl-2 protein was significantly lower in
the hyperthermia with seizure animals than that of the sham-control and
hyperthermia without seizure groups. The expression of pro-apoptotic Bax
protein also significantly increased in the hippocampus of hyperthermia with
seizure group rats compared to the sham-control and hyperthermia without
seizure animals.
Conclusion
The simple febrile seizure markedly disturbed the hippocampal expression of
both Bcl2 and Bax proteins, resulting in apoptosis promotion in hippocampi of
juvenile rats, which were measurable for at least 15 days.