Effects of Nigella sativa on apoptosis and GABA(A) receptor density in cerebral cortical and hippocampal neurons in pentylenetetrazol induced kindling in rats


Meral I. , Esrefoglu M. , Dar K. A. , Ustunova S. , Aydın M. S. , Demırtas M., et al.

BIOTECHNIC & HISTOCHEMISTRY, cilt.91, ss.493-500, 2016 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 91
  • Basım Tarihi: 2016
  • Doi Numarası: 10.1080/10520295.2016.1245866
  • Dergi Adı: BIOTECHNIC & HISTOCHEMISTRY
  • Sayfa Sayısı: ss.493-500

Özet

We investigated the effects of Nigella sativa on apoptosis and gamma-aminobutyric acid (GABA(A)) receptor density in cerebral cortical and hippocampal neurons in a pentylenetetrazol (PTZ)-induced kindling model in rats. The PTZ kindling model was produced by injecting PTZ in subconvulsive doses to rats on days 1, 3, 5, 8, 10, 12, 15, 17, 19, 22 and 24 of the study into animals of PTZ treated (PTZ) and PTZ + N. sativa treated (PTZ + NS) groups. Clonic and tonic seizures were induced by injecting a convulsive dose of PTZ on day 26 of the study. Rats in the PTZ + NS group were treated also with a 10 mg/kg methanolic extract of N. sativa 2 h before each PTZ injection. Rats in the control group were treated with 4 ml/kg saline. The number of neurons that expressed GABA(A) receptors in the hippocampus and cerebral cortex of rats in the PTZ and PTZ + NS groups increased significantly. There was no significant difference in the number of GABA(A) receptors between the PTZ and PTZ + NS groups. GABA(A) receptor density of the neurons in the cerebral cortex, but not hippocampus, was increased in PTZ group compared to controls. We observed a significant increase in the number of apoptotic neurons in the cerebral cortex of rats of both the PTZ and PTZ + NS groups compared to controls. We observed a significant decrease in the number of the apoptotic neurons in the cerebral cortex of rats in the PTZ + NS group compared to the PTZ group. N. sativa treatment ameliorated the PTZ induced neurodegeneration in the cerebral cortex as reflected by neuronal apoptosis and neuronal GABA(A) receptor frequency.