الفهرس 
Cerebral frontal cortexOnly 14 pages are availabe for public view
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Abstract
The central nervous system is vulnerable to complications caused by
diabetes mellitus. Diabetes causes degenerative effects and stimulates
apoptosis on pyramidal cells of layer III in the frontal cerebral cortex. Also,
it has the same effect in the hippocampal CA1 region which may impair its
homeostasis and function. Therefore, layer III of cerebral frontal cortex and
CA1 region were chosen for this study.
Nigella Sativa has been reported to possess antidiabetic activity. The
consumption of NS seed and its active constituents may decrease the rate of
neurodegenerative diseases. The protective effect of NS has been attributed
to its strong antioxidant properties, which are related to its ability to
scavenge various reactive oxygen species, including superoxide radical
anion and hydroxyl free radicals, to block lipid peroxidation and to enhance
antioxidant enzymes
The present work aimed to study and evaluated the neuroprotective
effect of nigella sativa extract on the frontal cortex and hippocampus in
experimentallyinduced diabetes mellitus in adult male albino rat. This was
based on biochemical, histological, immunohistochemical and
morphometric analyses.
Thirty -six healthy adult male albino rat weighing 200-250g were used
in this study. The animals were divided into five groups:
group I (Control group): composed of 12 animals which were subdivided
into 2 subgroups:
•Subgroup Ia: (Plain control): Included 6 animals which were kept without
any treatment all over the experimental period.
• Subgroup Ib: (Sham control): Included 6 animals each received a single
dose of intraperitoneal injection of 0.1M sodium citrate buffer pH 4.5(the solvent of STZ).
group II (Nigella Sativa (NS) group): Included 6 animals each, was given
Nigella Sativa extract in the onset of the experiment (200 mg/kg) dissolved
in distilled water orally by a gavage tube daily for 6 weeks.
group III (Diabetic group): Included 6 animals, each was given a 50
mg/kg, single intraperitoneal (I/p) injection of streptozotocin (STZ) till
diagnosis of DM was done then the animals were followed until the end of
the experiment.
group IV (NS-Protected group): Included 6 animals, each received NS
extract 200 mg/kg/day orally by a gavage tube for three weeks before
induction and diagnosis of DM and continue receiving the same dose for
another 3 weeks.
group V (NS-Treated group): Included 6 animals so diabetes was first
induced in each animal by a 50 mg/kg, single I/p injection of STZ till
diagnosis of DM then they received NS extract 200 mg/kg orally by a
gavage tube daily for 6 weeks.
After 6 weeks from the onset of the experiment each rat was anaesthetized
using diethyl ether inhalation, blood samples were collected from the retroorbital venous plexus for assay of serum levels of blood glucose and MDA.
And then their brains were dissected and subjected to histological and
immunohistochemical assessment using:
1. Haematoxylin & Eosin stain (Hx & E).
2. Toulidine blue stain.
3. Immunohistochemical staining of GFAP, Ki67, Caspase-3 and iNOS.
Morphometric measurements were done by the image analyzer for color
intensity of Nissl’s granules, number of GFAP immunopositive cells, number
of Ki-67 immunopositive cells, number of Caspase-3 immunopositive cells and the number of iNOS immunopositive cells.
Statistical analysis was done for all calculated parameters.