Effects of Ginkgo biloba Extract on Spinal Cord Ischemia–Reperfusion Injury in Rats

Badem, Serdar; Uğurlucan, Murat; El, Helin; Şahın, Mazlum; Uysal, Müjdat; Sayın, Ömer Ali; Gürel, Bora; Başaran, Murat; Bayindir, Çiçek; Alpagut, Ufuk; Dayıoğlu, Enver

doi:10.1016/j.avsg.2014.02.020

Cited by 10 publications

(23 citation statements)

References 23 publications

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“…Neurotoxicity, intracellular calcium increase, lipid peroxidation, and free radical formation are all part of a complex relationship in the pathophysiology of spinal cord ischemia. Reperfusion restores lost cellular functions during ischemia; however, it increases blood flow and tissue oxygenation and thereby causes further damage in ischemic tissues via the formation of reactive oxygen radicals [47]. Besides triggering cell damage, oxidative stress has also been shown to be a trigger of autophagy activation in neuronal cells [33].…”

Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Inhibits Autophagic Neuronal Cell Death by Reducing Oxidative Stress in Spinal Cord Ischemia Reperfusion Injury

Xie

Yang

et al. 2017

Oxidative Medicine and Cellular Longevity

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Autophagy is upregulated in spinal cord ischemia reperfusion (SCIR) injury; however, its expression mechanism is largely unknown; moreover, whether autophagy plays a neuroprotective or neurodegenerative role in SCIR injury remains controversial. To explore these issues, we created an SCIR injury rat model via aortic arch occlusion. Compared with normal controls, autophagic cell death was upregulated in neurons after SCIR injury. We found that autophagy promoted neuronal cell death during SCIR, shown by a significant number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling- (TUNEL-) positive cells colabeled with the autophagy marker microtubule-associated protein 1 light chain 3, while the autophagy inhibitor 3-methyladenine reduced the number of TUNEL-positive cells and restored neurological and motor function. Additionally, we showed that oxidative stress was the main trigger of autophagic neuronal cell death after SCIR injury and N-acetylcysteine inhibited autophagic cell death and restored neurological and motor function in SCIR injury. Finally, we found that hydrogen sulfide (H2S) inhibited autophagic cell death significantly by reducing oxidative stress in SCIR injury via the AKT-the mammalian target of rapamycin (mTOR) pathway. These findings reveal that oxidative stress induces autophagic cell death and that H2S plays a neuroprotective role by reducing oxidative stress in SCIR.

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Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Inhibits Autophagic Neuronal Cell Death by Reducing Oxidative Stress in Spinal Cord Ischemia Reperfusion Injury

Xie

Yang

et al. 2017

Oxidative Medicine and Cellular Longevity

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“…In a rabbit model of SCIRI, the intraperitoneal administration of curcumin just after the onset of reperfusion has been proved to relief the spinal cord ischemia injury [60]. Kurt et al [61] indicated that in a rat model of SCIRI the treatment withn 100 mg/kg/day orogastric dose of Ginkgo biloba extract for 3 days pre-surgery and 2 days post-surgery, which led to attenuate spinal cord ischemia injury. However, even if several studies aimed to verify the protective effect of traditional Chinese medicine have been conducted on murine, rat and rabbit models, the analysis of these effects on human cohort is lacking.…”

Section: Traditional Chinese Medicinementioning

confidence: 98%

Targeting the blood-spinal cord barrier: A therapeutic approach to spinal cord protection against ischemia-reperfusion injury

Xie

et al. 2016

Life Sciences

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“…The work of Badem et al [42] evaluated the effect of EGB761 in medullar ischemia. For that, researched clamped the infrarenal abdominal aorta in mice, which were divided into groups, and values of MDA, SOD, GSH, and GPx tissue, as well as tissue from spinal cord samples, were analyzed.…”

Section: Compound Action Referencesmentioning

confidence: 99%

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2020

Planta Med

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ABSTR AC TGinkgo biloba (GB) is one of the most widely used phytotherapeutic products in the world, and its extract has beneficial properties for the treatment of several pathologies, such as diabetic cardiomyopathy, neurodegenerative diseases, cataracts, hearing loss, myocardial lesion, hippocampus neuronal lesions, morphometry testicular changes, and liver damage. This review aims to investigate the effects of GB on diseases related to oxidative stress. Databases such as MEDLINE/ PUBMED and EMBASE were consulted, and PRISMA guidelines were used to build the review. This plant has antioxidant properties since it regulates the expression of antioxidant enzymes positively and reduces reactive oxygen and nitrogen species, contributing to the reduction of lipid peroxidation. It also exhibits anti-inflammatory properties, inhibiting the expression of pro-inflammatory cytokines, such as IL-1, IL-6, and TNF-α. In animal models, the use of GB can show positive effects on brain damage, neurodegenerative diseases, myocardial injury, and renal and liver damage. In humans, the positive effects were shown in diabetes, metabolic syndrome, and ischemic colitis. These effects are due to the presence of compounds such as bilobalide, isoramnetina, quercetin, kaempferol, and ginkgolides A, B, and C. For these reasons, GB can be a lowcost alternative to the therapeutic approach of several pathologies since it acts in the prevention, treatment, and inhibition of several complications of common comorbidities.

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Effects of Ginkgo biloba Extract on Spinal Cord Ischemia–Reperfusion Injury in Rats

Cited by 10 publications

References 23 publications

Hydrogen Sulfide Inhibits Autophagic Neuronal Cell Death by Reducing Oxidative Stress in Spinal Cord Ischemia Reperfusion Injury

Hydrogen Sulfide Inhibits Autophagic Neuronal Cell Death by Reducing Oxidative Stress in Spinal Cord Ischemia Reperfusion Injury

Targeting the blood-spinal cord barrier: A therapeutic approach to spinal cord protection against ischemia-reperfusion injury

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