AI Article Synopsis
- Various antiepileptic drugs, particularly those that induce enzymes, might increase vascular risks by impairing the body’s natural antioxidant abilities, leading to tissue damage; however, the effects of the non-enzyme-inducing drug lamotrigine (LTG) on oxidative stress have been less studied.
- A study was conducted using male Wister rats divided into four groups to investigate the impact of LTG on vascular risk factors in a model of seizures, examining levels of lipoproteins, homocysteine, malondialdehyde, and glutathione over five weeks.
- Results indicated that epileptic rats exhibited higher levels of harmful substances and lower beneficial lipoproteins compared to controls, but LTG treatment resulted in improved seizure severity
Article Abstract
Various antiepileptic drugs (AEDs) especially enzyme-inducing AEDs might be associated with increased vascular risk, through impairment of the endogenous antioxidative ability which may trigger oxygen-dependent tissue injury. Lamotrigine (LTG) a non-enzyme-inducing AED has scarce information regarding its effects on oxidative stress. The present study aimed to study the possible modulation of vascular risk factors of epileptogenesis by LTG, in a rat model of kindling seizure induced by pentylenetetrazole (PTZ). Four groups of male Wister rats were used; vehicle control group, PTZ group (alternate day PTZ, 30 mg/kg, i.p), LTG/PTZ group (LTG 20 mg/kg/day p.o and alternate day PTZ) and LTG group. The study period was 5 weeks. Lipoproteins and total homocysteine (tHcy), malondialdehyde (MDA) and reduced glutathione (GSH) were measured. Aortic endothelial function study and histopathological examination of the rats' brains, aortas and coronaries were conducted. Serum total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C), tHcy, MDA, GSH levels were significantly higher in epileptic rats than normal controls rats. A decrease in HDL-cholesterol with high atherosclerotic index was also demonstrated. The administration of LTG improved the PTZ-kindled seizures. It produced a significant decrease in TC, TG and LDL-cholesterol, MDA, aortic GSH and increase in HDL-cholesterol with no significant effect on serum GSH and tHcy levels. LTG improved endothelium-dependent relaxation, decreased hippocampal neurodegenerative changes and atherosclerotic changes of aortas and coronaries. LTG decreased seizures severity, hippocampal damage and improved vascular risk markers in this rat model of kindling seizures.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4071181 | PMC |
| http://dx.doi.org/10.4196/kjpp.2014.18.3.269 | DOI Listing |
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