Neuroprotective Effect of Curcumin on Kainic Acid Model of Epilepsy in Male Swiss Albino Mice
International Journal of Chemical and Natural Science • 2016
معلومات البحث
المؤلفون
Samy Ali Hussein, Afaf D. Abdel-mageid, Omnia M. Abd-Elhamed, Aziza Amin andHassan S . Al-Harthy
الكلمات المفتاحية
Curcumin, kainic acid, epilepsy, apoptosis; antioxidant enzymes, caspase-3, histopathology
المجلة العلمية
International Journal of Chemical and Natural Science
الناشر
Aizeon publishers
المجلد
4
العدد
4
الصفحات
447-460
publication.type
International
رابط البحث
Open Link
المواد المرفقة
Not Available
الملخص
Oxidative stress resulting from excessive free-radical release is likely implicated in the initiation and progression of
epilepsy. The potential neuroprotective effect of curcumin (CUR) on KA-induced epilepsy in mice was evaluated.
Twenty four male Swiss Albino mice were divided into four groups. Group Ι:(Control group) mice received no drugs.
Group Π:(epilepsy-induced group): mice administered with a single dose of KA (10 mg/kg b.wt) intraperitoneally
(i.p). Group III:(epilepsy+ CUR protected group) mice received CUR (200 mg/kg b.wt/day/orally) for 7 days before
KA administration. Group IV:(epilepsy+ CUR treated group): mice first injected with KA(10 mg/kg b.wt/i.p.) then
after 15 min. CUR was administered as in group III for 3 consecutive days. The obtained results showed that, KAinduced epilepsy in mice caused significant decrease in serum sialic acid (SA), and brain tissue SOD, CAT, GPx
activities and GSH concentration. However, serum TNF-α , IL-1β and brain tissue nitric oxide NO, L-MDA levels,
caspase-3, DNA-fragmentation, 8-hydroxy-2-deoxyguanosine 8-OHdG, activator protein-1 activator protein-1 AP-1
and Myeloperoxidase MPO were significantly increased. Administration of CUR was able to mitigate KA- induced
epilepsy through rising of serum SA and brain tissue enzymatic antioxidants status and GSH and declining NO, LMDA, caspase-3, DNA-fragmentation, 8-OHdG, AP-1 and MPO in brain tissue. The microscopical examination of
brain tissues obtained from rats injected with KA showed variable pathological changes represented mainly in
hemorrhage, edema, neural degeneration and encephalomalacia. Meanwhile, curcumin injection was able to reduce
the severity of these alterations with variable degree especially in epilepsy+curcumin treated group. These results
suggest that, CUR may be successful in the treatment of epilepsy by its radical scavenging, anti-inflammatory and
antiapoptotic activities and regenerating endogenous antioxidant mechanism. Also, curcumin protects mice brain
against KA induced neuronal damage, decrease the severity of epilepsy and attenuated kainite induced
inflammation and apoptosis
epilepsy. The potential neuroprotective effect of curcumin (CUR) on KA-induced epilepsy in mice was evaluated.
Twenty four male Swiss Albino mice were divided into four groups. Group Ι:(Control group) mice received no drugs.
Group Π:(epilepsy-induced group): mice administered with a single dose of KA (10 mg/kg b.wt) intraperitoneally
(i.p). Group III:(epilepsy+ CUR protected group) mice received CUR (200 mg/kg b.wt/day/orally) for 7 days before
KA administration. Group IV:(epilepsy+ CUR treated group): mice first injected with KA(10 mg/kg b.wt/i.p.) then
after 15 min. CUR was administered as in group III for 3 consecutive days. The obtained results showed that, KAinduced epilepsy in mice caused significant decrease in serum sialic acid (SA), and brain tissue SOD, CAT, GPx
activities and GSH concentration. However, serum TNF-α , IL-1β and brain tissue nitric oxide NO, L-MDA levels,
caspase-3, DNA-fragmentation, 8-hydroxy-2-deoxyguanosine 8-OHdG, activator protein-1 activator protein-1 AP-1
and Myeloperoxidase MPO were significantly increased. Administration of CUR was able to mitigate KA- induced
epilepsy through rising of serum SA and brain tissue enzymatic antioxidants status and GSH and declining NO, LMDA, caspase-3, DNA-fragmentation, 8-OHdG, AP-1 and MPO in brain tissue. The microscopical examination of
brain tissues obtained from rats injected with KA showed variable pathological changes represented mainly in
hemorrhage, edema, neural degeneration and encephalomalacia. Meanwhile, curcumin injection was able to reduce
the severity of these alterations with variable degree especially in epilepsy+curcumin treated group. These results
suggest that, CUR may be successful in the treatment of epilepsy by its radical scavenging, anti-inflammatory and
antiapoptotic activities and regenerating endogenous antioxidant mechanism. Also, curcumin protects mice brain
against KA induced neuronal damage, decrease the severity of epilepsy and attenuated kainite induced
inflammation and apoptosis
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