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RISS 인기검색어
- 검색키워드
- 저자 : Basma S Haggag (검색결과 2 건)
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Haggag, Basma S.,Hasanin, Amany H.,Raafat, Mona H.,Kawy, Hala S. Abdel The Korean Society of Pharmacology 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.3
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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Basma S Haggag,Amany H Hasanin,Mona H Raafat,Hala S Abdel Kawy 대한약리학회 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.3
Various antiepileptic drugs (AEDs) especially enzyme-inducing AEDs might be associated withincreased vascular risk, through impairment of the endogenous antioxidative ability which may triggeroxygen-dependent tissue injury. Lamotrigine (LTG) a non-enzyme-inducing AED has scarce informationregarding its effects on oxidative stress. The present study aimed to study the possible modulationof vascular risk factors of epileptogenesis by LTG, in a rat model of kindling seizure induced bypentylenetetrazole (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 studyand histopathological examination of the rats’ brains, aortas and coronaries were conducted. Serumtotal 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 inHDL-cholesterol with high atherosclerotic index was also demonstrated. The administration of LTGimproved 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 tHcylevels. LTG improved endothelium-dependent relaxation, decreased hippocampal neurodegenerativechanges 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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