Lipid peroxide, phospholipids, glutathione levels and superoxide dismutase activity in rat brain after ischaemia: Effect of ginkgo biloba extract

Seif-El-Nasr, Mona; El-Fattah, Amal Ahmed Abd

doi:10.1016/s1043-6618(05)80014-3

Cited by 81 publications

(39 citation statements)

References 41 publications

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“…In the present study, SOD levels did not differ among groups. This is not consistent with some reports of cerebral I/R studies [42,43,44]. However, there are conflicting reports.…”

Section: Discussioncontrasting

confidence: 91%

Protective Effects of Minocycline against Short-Term Ischemia-Reperfusion Injury in Rat Brain

Aras¹,

Urfalı²,

Serarslan³

et al. 2013

Pediatr Neurosurg

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The aim of this study was to assess the effects of minocycline on cerebral ischemia-reperfusion (I/R) injury in rats. The study was carried out on 24 male Wistar albino rats, weighing 200-250 g, which were divided into three groups: (i) control (n = 8), (ii) I/R (n = 8) and (iii) I/R + minocycline (n = 8). Minocycline was administrated at a dose of 90 mg/kg p.o. to the I/R group 48, 24 and 1 h before ischemia. Following bilateral exposure of the common carotid arteries by anterior cervical dissection and separation of the vagus nerve, I/R injury was performed by occlusion. Following reperfusion, malondialdehyde (MDA), superoxide dismutase, glutathione peroxidase and catalase levels in the blood and brain tissue, and creatine kinase (CK), CK-BB, lactate dehydrogenase (LDH), neuron-specific enolase (NSE) and protein S100β levels in the blood were measured and the histopathological changes were monitored. Regarding histopathological evaluation, symptoms of degeneration were significantly improved in the I/R + minocycline group compared to the I/R-only group. Statistical analysis of the biochemical parameters revealed significant differences in MDA (p < 0.001), nitric oxide (p < 0.05), CK (p < 0.05) and CK-MB (p < 0.05) levels between the I/R + minocycline group and the I/R group. According to the literature, the effect of minocycline is firstly assessed by LDH, CK-MB, NSE and S-100β analysis in addition to antioxidant status and histopathological analysis.

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“…In the present study, SOD levels did not differ among groups. This is not consistent with some reports of cerebral I/R studies [42,43,44]. However, there are conflicting reports.…”

Section: Discussioncontrasting

confidence: 91%

Protective Effects of Minocycline against Short-Term Ischemia-Reperfusion Injury in Rat Brain

Aras¹,

Urfalı²,

Serarslan³

et al. 2013

Pediatr Neurosurg

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“…The rationale behind testing EGb in AD derives from its polyvalent mode of action [4]: EGb is (1) a free radical scavenger and an antioxidant, (2) a platelet-activating factor antagonist, (3) a vasomodulator and (4) an energy enhancer. Directly or indirectly related to these effects, EGb decreases lipid peroxidation [19] and protects hippocampal neurons against cell death induced by ß-amyloid [20]. Furthermore, EGb restores receptor density, particularly increasing the number of hippocampal muscarinic acetylcholine [21] and cortical 5-hydroxytryptamine 1A receptors [22], while enhancing high-affinity choline uptake [23].…”

Section: Drug Informationmentioning

confidence: 99%

Influence of the Severity of Cognitive Impairment on the Effect of the <i>Ginkgo biloba</i> Extract EGb 761<sup>®</sup> in Alzheimer’s Disease

Velasco²,

et al. 2002

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Objective: To explore the treatment effect of EGb 761^® (EGb) in Alzheimer’s disease depending on baseline severity. Methods: We applied stratification to the intent-to-treat data set collected during a 52-week, randomized, double-blind, placebo-controlled, parallel-group, multicenter study with 120 mg of EGb, using cutoff points of 23 and 14 for the Mini-Mental State Examination (MMSE) score. Outcome measures used were the cognitive subscale of the Alzheimer’s Disease Assessment Scale (ADAS-Cog) and the Geriatric Evaluation by Relative’s Rating Instrument (GERRI). Results: In the severity stratum 1 (MMSE >23), the placebo group did not show significant changes, while the EGb group improved significantly by 1.7 points on the ADAS-Cog and by 0.09 points on the GERRI. In the severity stratum 2 (MMSE <24), the placebo group worsened by 4.1 points on the ADAS-Cog and 0.18 points on the GERRI, whereas the EGb group showed 60% less decline on the ADAS-Cog (treatment difference of 2.5 points) and no change on the GERRI (treatment difference of 0.25 points). The most severely impaired subgroup (MMSE <15) showed slightly more pronounced worsening for both treatment groups. However, in comparison to placebo, EGb induced virtually the same magnitude of effect as was observed in the entire stratum 2. Conclusions: The results of this retrospective analysis indicated that a treatment effect favorable to EGb could be observed with respect to cognitive performance (p = 0.02) and social functioning (p = 0.001) regardless of the stage of dementia, whether mild or moderately severe. However, the relative changes from baseline measured at endpoint depended heavily on the severity at baseline. Improvement was observed in the group of patients with very mild to mild cognitive impairment, while in more severe dementia, the mean EGb effect should be considered more in terms of stabilization or slowing down of worsening, as compared to the greater deterioration observed with placebo.

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“…Por outro lado, os resultados de outros autores 13,16 , revelaram aumento dos lipoperóxidos cerebrais, após curtos períodos de reperfusão. Muitos outros estudos mostraram também alterações significativas do MDA em fases precoces de reperfusão: Vagnozzi e col. (1994 e 1995), Seifel-Nars e El-Fattah (1995) e Siragusa e col. (1997) verificaram haver aumento significativo de MDA em ratos submetidos à isquemia e reperfusão cerebral, quando comparados aos grupos controle sem isquemia e reperfusão 34,35,36,37 . Foi com base nos resultados desses estudos que, no presente experimento, optou-se pelas dosagens de MDA nas fases mais precoces da reperfusão (uma e duas horas).…”

Section: Discussionunclassified

Avaliação de dois modelos experimentais de isquemia e reperfusão cerebral em ratos com oclusão temporária carotídea associada ou não à oclusão vertebral

et al. 2003

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A doença aterosclerótica das artérias carótidas pode provocar sintomas como amaurose fugaz, cefaléia ou acidente isquêmico transitório (AIT). O quadro clínico mais temido é o acidente vascular cerebral (AVC), não apenas pelas seqüelas incapacitantes que podem ocorrer, mas principalmente, pelo risco de óbito; sabese que, nos Estados Unidos, o AVC é a terceira causa mais freqüente de morte. Deve-se ressaltar que, no primeiro ano após a ocorrência de um episódio de AIT, há um risco de, aproximadamente, 10% de o paciente vir a apresentar AVC. Também é importante ressaltar que, os pacientes assintomáticos e portadores de estenose carotídea maior ou igual a 75% têm um risco de 3 a 5% de virem a apresentar AVC, por ano de seguimento 1, 2 . Métodos: 60 ratos foram distribuídos, aleatoriamente, em três grupos experimentais, com 20 animais cada: I -pinçamento temporário de artéria carótida esquerda; II -cauterização prévia das artérias vertebrais e pinçamento temporário da artéria carótida esquerda; simulado -sem isquemia nem reperfusão. Todos os animais tiveram oclusão definitiva de artéria carótida direita e os três grupos foram subdivididos em dois períodos de reperfusão: A -60 minutos e B -120 minutos. Os parâmetros verificados foram: medidas de pressão arterial média sistêmica e fluxo sangüíneo carotídeo; medida de malondialdeído cerebral através do teste TBARS e avaliação histológica do hemisfério cerebral submetido à isquemia e reperfusão. Foi feito também um estudo complementar com angiografia cerebral em 5 animais adicionais. Resultados: Não houve diferenças significativas nas dosagens de malondialdeído cerebral e na freqüência e gravidade das alterações histológicas cerebrais entre os três grupos. Nos grupos GI e GII, a PAM foi significantemente maior no período de isquemia. O fluxo sangüíneo entre os períodos pré e pós-pinçamento aumentou nos grupos IA e IIB, diminuiu no grupo IB e no grupo IIA manteve-se inalterado. As angiografias do estudo complementar mostraram aporte sangüíneo para cérebro através de circulação colateral. Conclusão: Os modelos de isquemia e reperfusão estudados não demonstraram alterações consistentes de marcadores de lesão cerebral, seja quanto à produção de lipoperóxidos ou de lesões histológicas. DESCRITORES -Isquemia e reperfusão cerebral. Lipoperoxidação.

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Lipid peroxide, phospholipids, glutathione levels and superoxide dismutase activity in rat brain after ischaemia: Effect of ginkgo biloba extract

Cited by 81 publications

References 41 publications

Protective Effects of Minocycline against Short-Term Ischemia-Reperfusion Injury in Rat Brain

Protective Effects of Minocycline against Short-Term Ischemia-Reperfusion Injury in Rat Brain

Influence of the Severity of Cognitive Impairment on the Effect of the <i>Ginkgo biloba</i> Extract EGb 761<sup>®</sup> in Alzheimer’s Disease

Avaliação de dois modelos experimentais de isquemia e reperfusão cerebral em ratos com oclusão temporária carotídea associada ou não à oclusão vertebral

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