The effect of gabapentin on oxidative stress in a model of toxic demyelination in rat brain.
J Basic Clin Physiol Pharmacol
; 23(2): 61-8, 2012.
Article
in En
| MEDLINE
| ID: mdl-23089532
ABSTRACT
BACKGROUND:
Gabapentin, a structural analog of γ-aminobutyric acid (GABA), is used in the treatment of neuropathic pain in multiple sclerosis.METHODS:
This study investigated the effect of gabapentin on oxidative stress in a model of brain demyelination evoked by intracerebral injection (i.c.i) of ethidium bromide (10 µL of 0.1%). Rats received saline (control) or gabapentin at 100 or 300 mg/kg orally daily for 10 days prior to injection of ethidium bromide. Rats were euthanized 1 day later, and then the levels of reduced glutathione (GSH), glutathione peroxidase (GPx) activity, lipid peroxidation (malondialdehyde; MDA), nitrite, acetyl cholinesterase (AChE) and paraoxonase activities were assessed in the brain cortex in different treatment groups.RESULTS:
Ethidium bromide resulted in increased oxidative stress in the cortex 1 day after its injection. Malondialdehyde increased by 30.2%, whereas GSH decreased by 17.6%. GPx activity was inhibited by 78.6%. Brain nitrite increased by 55.4%, AChE activity decreased by 33.4% and paraoxonase activity decreased by 27.5%. In ethidium bromide treated rats, gabapentin administered at 300 mg/kg increased cortical MDA by 66%. GSH was unaltered by gabapentin, but GPx activity decreased by 54.3% by the higher dose of gabapentin. Nitrite decreased by 21.4% and 29.2% after 100 and 300 mg/kg of gabapentin, respectively. AChE activity increased by 28.6% and 69.3% by 100 and 300 mg/kg of gabapentin, respectively. Paraoxonase activity showed 83.3% and 73% decreases by 100 and 300 mg/kg of gabapentin, respectively.CONCLUSIONS:
These results suggest that gabapentin increases brain lipid peroxidation and decreases brain antioxidant enzymes in this model of chemical demyelination.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Demyelinating Diseases
/
Oxidative Stress
/
Excitatory Amino Acid Antagonists
/
Cyclohexanecarboxylic Acids
/
Gamma-Aminobutyric Acid
/
Amines
Limits:
Animals
Language:
En
Journal:
J Basic Clin Physiol Pharmacol
Journal subject:
FARMACOLOGIA
/
FISIOLOGIA
Year:
2012
Type:
Article
Affiliation country:
Egypt