NADPH-diaphorase activity in the spinal cord after ischemic injury and the effects of pretreatment with Ginkgo biloba extract (EGb 761)

Mechírová, Eva; Domoráková, Iveta

doi:10.1078/0065-1281-00662

Cited by 15 publications

(14 citation statements)

References 14 publications

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“…In our previous study we described the more resistant nitrergic neurons in the dorsal horns and pericentral area of the spinal cord after ischemia/reperfusion and NADPH-d histochemistry (Mechírová and Domoráková, 2002). Vulnerable neurons in the intermediate zone and ventral horns remained NADPH-d negative.…”

Section: Discussionmentioning

confidence: 95%

Extract EGb 761 Pretreatment Limits Ubiquitin Positive Aggregates in Rabbit Spinal Cord Neurons after Ischemia-Reperfusion

2006

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1. Ubiquitin immunohistochemistry was used for investigation of time dependent changes of ubiquitin in the nerve cells reacting to ischemic/reperfusion damage. In the rabbit spinal cord ischemia model a period of 30 min ischemia followed by 24 and 72 h of reperfusion caused neuronal degeneration selectively in the ventral horn motor neurons as well as interneurons of the intermediate zone. 2. Ubiquitin aggregates were accumulated in the neurons of lamina IX and the neurons of intermediate zone destined to die 72 h after 30 min of the spinal cord ischemia. 3. The activation of ubiquitin hydrolytic system is related to a defective homeostasis and could trigger different degenerative processes. Having in mind this, we used EGb 761 to rescue the motor neurons and interneurons against ischemia/reperfusion damage. Our results show that after 30 min of ischemia and 24 or 72 h of reperfusion with EGb 761 pre-treatment for 7 days the vulnerable neurons in the intermediate zone and lamina IX exhibit marked elevation of ubiquitin-positive granules in the cytoplasm, dendrites and nuclei. Abnormal protein aggregates have not been observed in these cells. 4. The rabbits were completely paraplegic after 30 min of ischemia and 24 or 72 h of reperfusion. However, after 7 days EGb 761 pre-treatment, 30 min of ischemia and 24 or 72 h of reperfusion the animals did not show paraplegia. 5. Evaluated ubiquitin-positive neurons of the L(5)-L(6) segments showed significant decrease in number and significant increase of density after 30 min of ischemia followed by 24 h and mainly 72 h of reperfusion. Ubiquitin immunohistochemistry confirmed the protective effect of EGb 761 against ischemia/reperfusion damage in the rabbit spinal cord.

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Section: Discussionmentioning

confidence: 95%

Extract EGb 761 Pretreatment Limits Ubiquitin Positive Aggregates in Rabbit Spinal Cord Neurons after Ischemia-Reperfusion

2006

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“…Bilobalide component of EGb 761 increases the respiratory control ratio of mitochondria and protects against the uncoupling of oxidative phosphorylation, by this way increases ATP levels (DeFeudis 2002), influences cognitive deficits that follow stress or traumatic brain injury (DeFeudis and Drieu 2000). Positive effects of EGb 761 pretreatment on neurons after ischemia/reperfusion were confirmed by studies of global ischemia in the rats (Hrehorovska et al 2004;Domorakova et al 2006) or in the gerbils (Chandrasekaran et al 2002) and in the rabbit spinal cord ischemia (Mechirova and Domorakova 2002;Mechirova et al 2006). Less data were found about ischemia/reperfusion and EGb 761 posttreatment.…”

Section: Introductionmentioning

confidence: 83%

Effect of Antioxidant Treatment in Global Ischemia and Ischemic Postconditioning in the Rat Hippocampus

et al. 2009

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Ischemic postconditioning is a very effective way how to prevent delayed neuronal death. Effect of Ginkgo biloba extract (EGb 761; 40 mg/kg) posttreatment was studied on the rat model of transient forebrain ischemia and ischemia/postconditioning. Global ischemia was produced by four-vessel occlusion in Wistar male rats. Two experimental protocols were used: (a) 10 min of ischemia/7 days of reperfusion with or without EGb 761 treatment or (b) 10 min of ischemia/2 days of reperfusion/5 min of ischemia (postconditioning), following 5 days of reperfusion. EGb 761 was applied as follows: 30 min before 10 min of ischemia then 5 h, 1 and 2 days after 10 min of ischemia. Fluoro Jade B, marker for neuronal degeneration, was used for quantitative analysis of the most vulnerable hippocampal CA1 neurons. Cognitive and memory functions were tested by Morris water maze, as well. Administration of EGb 761 30 min before 10 min of ischemia or 5 h after ischemia has rather no protective effect on neuronal survival in CA1 region. Ten minutes of ischemia following ischemic postconditioning after 2 days of reperfusion trigger a significant neuroprotection of CA1 neurons, but it is abolished by EGb 761 posttreatment. Ischemia/postconditioning group showed a significant improvement of learning and memory on the seventh day of reperfusion. Protection of the most vulnerable CA1 neurons after ischemia/postconditioning is abolished by exogenous antioxidant treatment used in different time intervals after initial ischemia. Moreover, combination of EGb 761 administration with repeated stress (5 min ischemia used as postconditioning) causes cumulative injury of CA1 neurons.

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“…In patients with mild cognitive impairment neuroprotective drugs according experimental results (Mechirova and Domorakova, 2004) are used. A large problem of clinical practice is late onset of therapy with inhibitors of acetylcholinesterase or memantin, which are the symptomatic and it seems also neuroprotective therapy for patients with AD.…”

Section: Discussionmentioning

confidence: 99%

Polymorphism of Apolipoproteine E in Relation with Alzheimer and Vascular Dementia

2006

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1. The epsilon 4 allele of the apolipoprotein E gene increases the risk of late onset familial and sporadic Alzheimer disease. Relation of epsilon 4 allele of the apolipoprotein E gene to various types of dementia and the onset of dementia were analyzed in the present study. 2. The study comprised 139 patients (50 men and 89 women) with dementia, mean age 73.61 years (range 47-98). The diagnosis of dementia was made according to Diagnostic and Statistical Manual of Mental Disorders, and subtypes diagnoses were made according to NINCDS-ADRDA and NINDS-AIREN criteria. Minimental State Examination (MMSE) was used for the screening of dementia. Apolipoprotein E polymorphism was determined by the PCR-RFLP technique-polymerase chain reaction and subsequent digestion with specific restriction endonuclease. For statistical analyses chi-square test and the crude Gart s odds ratio (OR) and 95% confidence intervals (CI) were used. 3. From 139 dementia patients (MMSE < or =24 points) in 61 (45%) Alzheimer disease (AD) was present, in 44 patients (31%) vascular dementia (VD), and in 34 (24%) mixed dementia (MD) were revealed. In comparison with control group the presence of at least one ApoE-varepsilon4 allele was significantly higher only in the group with AD (p < 0.001), (OR=2.76; 95%: 1.42-5.36). The frequency of epsilon4 allele carriers was significantly overrepresented in AD group compared with VD (chi(2)=5.94; p=0.0148). Differences between AD and MD or VD and MD were not confirmed.

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NADPH-diaphorase activity in the spinal cord after ischemic injury and the effects of pretreatment with Ginkgo biloba extract (EGb 761)

Cited by 15 publications

References 14 publications

Extract EGb 761 Pretreatment Limits Ubiquitin Positive Aggregates in Rabbit Spinal Cord Neurons after Ischemia-Reperfusion

Extract EGb 761 Pretreatment Limits Ubiquitin Positive Aggregates in Rabbit Spinal Cord Neurons after Ischemia-Reperfusion

Effect of Antioxidant Treatment in Global Ischemia and Ischemic Postconditioning in the Rat Hippocampus

Polymorphism of Apolipoproteine E in Relation with Alzheimer and Vascular Dementia

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