POTENTIAL ROLE OF NITRIC OXIDINEXPERIMENTALPILOCARPINE-INDUCEEPILEPSY IN ADULTMALEALBINO RATS EPILEPSY ANDNITRICOXIDE
DOI:
https://doi.org/10.48047/Keywords:
Epilepsy,Pilocarpine,Aminoguanidine,induciblenitricoxidesynthase(iNOS),tumornecrosisfactoralpha(T NF-α).Abstract
Epilepsy is the most common serious neurological condition affecting 1 to 2 %
ofworldpopulation.Despite extensiveprogress,thereare still manyunansweredquestionsabout factors inducing
epilepsy. Therefore, this work was carried out in an attempt to studythe effect of nitric oxide (NO) modulation
on the development of epilepsy. Rats were dividedinto the following equal groups (8 rats each) according to
treatment;Controlnontreated;Pilocarpinetreated;Pilocarpine+Diazepamtreated;Pilocarpine+Aminoguanidine(asel
ective inhibitor of inducible nitric oxide synthase; (iNOS) treated groups. Twenty-fourhours' rat observation and
biochemical analysis of brain homogenates and serum showed thatPilocarpine induced seizures in all rats with
high lethality associated with increased brainexcitatory transmitter; glutamate, Gamma aminobutyric acid
(GABA), oxidative stress andNO,withincreasedseruminflammatorymediatorsastumornecrosisfactor(TNFα).Complete protection was observed with Diazepam without reversal of Pilocarpine-inducedbrain excitatory
transmitters changes apart from a significantly higher GABA levels but
withreducedlevelsofbrainNO,MDA,andserumTNF-αlevels.Ontheotherhand,Aminoguanidine was protective and
reversed all the Pilocarpine induced biochemical as wellas histological changes. In conclusion, although the role
ofNOinthepathophysiology
ofepilepsyiscontroversial,ourresultsshowedthatblockingiNOSwithAminoguanidineprovedtobeprotective,opening
thewayforanewstrategyofantiepilepticmanagement.
