Protective Effect of Ginkgolide B on High Altitude Cerebral Edema of Rats

Yu, Bo; Ma, Jie; Xiao, Wenjing; Xiang, Qingyu; Fan, Kun; Hou, Jing; Wu, Juan; Jing, Weihua

doi:10.1089/ham.2012.1080

Cited by 20 publications

(6 citation statements)

References 14 publications

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“…In another study conducted in WAG/Rij rats, it was determined that 1%, 10%, and 30% DMSO injections had no effect on absence seizures in all recording periods (Kovács et al, 2011). The doses and the routes of administration of the active components of EGb 761 have been determined according to the literature (Botao et al, 2013; Huang et al, 2012; Shah et al, 2011). These chemicals were injected intracerebroventricularly (i.c.v.)…”

Section: Methodsmentioning

confidence: 99%

Investigating the mechanism of action of ginkgolides and bilobalide on absence seizures in maleWAG/Rij rats

Gedikli

Akça

Yıldırım

2023

J of Neuroscience Research

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The effects of a single and multiple doses of ginkgolide A, B, C, and bilobalide, active components of Ginkgo biloba extract (EGb 761), on absence seizures were investigated in male WAG/Rij rats, a genetic animal model of absence epilepsy. Furthermore, the interactions of ginkgolide A together with NMDA receptor antagonist MK-801, AMPA/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), or L-type calcium channel blocker nicardipine were studied to figure out how ginkgolide A affects spike-wave discharges (SWDs) in the brain. The experiments were done using 6-8-month-old male WAG/Rij rats with infusion cannula and EEG electrode implanted. Ginkgolide A, B, C, and bilobalide were administered intraperitoneally for 7 days at a dose of 6 mg/kg. In interaction groups, 6 μg ginkgolide A was injected intracerebroventricularly in combination with MK-801 (10 μg), CNQX (1 μg), and nicardipine (50 μg) for 7 days. EEG was recorded from animals at the baseline, first dose, and seventh dose periods for 4 h. Ginkgolide A (p = .028), C (p = .046), and bilobalide (p = .043) significantly increased the frequency of SWDs in WAG/Rij rats. Ginkgolide A injected into the lateral ventricle with MK-801 (p = .046), CNQX (p = .043), and nicardipine (p = .046) significantly increased the number of SWDs after seventh dose. Finally, the EGb 761-related increase in absence epilepsy was determined to be caused by ginkgolide A, C, and bilobalide. All three receptor antagonists/channel blockers do not inhibit the pro-absence effect of ginkgolide A. The findings revealed that ginkgolide A's pro-absence effect is mediated by brain circuits other than ionotropic glutamate receptors or L-type calcium channels.

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Section: Methodsmentioning

confidence: 99%

Investigating the mechanism of action of ginkgolides and bilobalide on absence seizures in maleWAG/Rij rats

Gedikli

Akça

Yıldırım

2023

J of Neuroscience Research

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“…Therefore, in recent years, there has been increasing attention to anti-inflammatory and antioxidant substances derived from a number of natural substances, especially traditional Chinese herbal medicines. Natural antioxidants such as ginkgolide B, 121 quercetin, 62 tetrahydrocurcumin, 100 areca polyphenols, 68 salidroside, 97 , 122 phenylethanol glycoside 99 and potentilla anserine L. polysaccharide 101 can reduce oxidative stress and inflammation in a hypobaric and hypoxic environment by enhancing the activity of antioxidant enzymes and inhibiting NF-κB inflammatory signaling, so as to prevent or treat HACE. In addition, endogenous Exendin-4 and ganglioside GM1 are also thought to alleviate HACE by inhibiting inflammation and oxidative stress ( Table 2 ).…”

Section: Study On Redox Homeostasis In the Treatment Of Hacementioning

confidence: 99%

“…The protective effect of GB may be related to its antioxidation and inhibition of caspase-dependent apoptosis pathway. [ 60 , 121 ] Ex-4 Isolated from the saliva secretion of the Gila monitor lizard Heloderma suspectum Polypeptide (enteric insulin-stimulating mimic peptide of 39 amino acids) (1) Ex-4 preconditioning can effectively inhibit inflammation and oxidative stress and alleviate brain injury by reducing the expression of IL-6, TNF-α and NF-κB in HACE model rats; (2) Ex-4 can increase the expression of VEGF and promote angiogenesis to maintain the integrity of blood-brain barrier, reduce brain water content and improve HACE in HACE model rats. [ 95 ] GM1 A ganglioside in the mammalian brain, found chiefly in neurons.…”

Section: Study On Redox Homeostasis In the Treatment Of Hacementioning

confidence: 99%

Progress in the Treatment of High Altitude Cerebral Edema: Targeting REDOX Homeostasis

Li¹,

Li²,

Luo³

et al. 2023

JIR

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With the increasing of altitude activities from low-altitude people, the study of high altitude cerebral edema (HACE) has been revived. HACE is a severe acute mountain sickness associated with exposure to hypobaric hypoxia at high altitude, often characterized by disturbance of consciousness and ataxia. As for the pathogenesis of HACE, previous studies suggested that it might be related to the disorder of cerebral blood flow, the destruction of blood-brain barrier and the injury of brain parenchyma cells caused by inflammatory factors. In recent years, studies have confirmed that the imbalance of REDOX homeostasis is also involved in the pathogenesis of HACE, which mainly leads to abnormal activation of microglia and destruction of tight junction of vascular endothelial cells through the excessive production of mitochondrial-related reactive oxygen species. Therefore, this review summarizes the role of REDOX homeostasis and the potential of the treatment of REDOX homeostasis in HACE, which is of great significance to expand the understanding of the pathogenesis of HACE. Moreover, it will also be helpful to further study the possible therapy of HACE related to the key link of REDOX homeostasis.

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“…Administration of GB 2 h after reperfusion effectively decreased infarction volume and brain edema in rats with MCAO (Fang et al 2010). Botao et al (2013) found that GB pretreatment reduced brain water content, increased superoxide dismutase activity and glutathione concentration, decreased MDA concentration, and decreased active caspase-3 and PARP expression in rats with high altitude cerebral edemas. GK, a derivate of GB, given at a higher dose also attenuated cerebral infarction and repressed brain edema formation in MCAO rats (Ma et al 2012).…”

Section: Mechanisms Of Ginkgolides and Bilobalide In Neuron Protectiomentioning

confidence: 99%

The neuroprotective mechanisms of ginkgolides and bilobalide in cerebral ischemic injury: a literature review

Feng

Sun

Chen

et al. 2019

Mol Med

101

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The incidence and mortality of strokes have increased over the past three decades in China. Ischemic strokes can cause a sequence of detrimental events in patients, including increased permeability and dysfunction of the blood-brain barrier, brain edema, metabolic disturbance, endoplasmic reticulum stress, autophagy, oxidative stress, inflammation, neuron death and apoptosis, and cognitive impairment. Thrombolysis using recombinant tissue plasminogen activator (rtPA) and mechanical embolectomy with a retrievable stent are two recognized strategies to achieve reperfusion after a stroke. Nevertheless, rtPA has a narrow therapeutic timeframe, and mechanical embolectomy has limited rates of good neurological outcomes. EGb761 is a standardized and extensively studied extract of Ginkgo biloba leaves. The ginkgolides and bilobalide that constitute a critical part of EGb761 have demonstrated protective properties towards cerebral injury. Ginkgolides include Ginkgolide A (GA), Ginkgolide B (GB), Ginkgolide C (GC), Ginkgolide J (GJ), Ginkgolide K (GK), Ginkgolide L (GL), and Ginkgolide M (GM). This review seeks to elucidate the neuroprotective effects and mechanisms of ginkgolides, especially GA and GB, and bilobalide in cerebral injury following ischemic strokes.

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Protective Effect of Ginkgolide B on High Altitude Cerebral Edema of Rats

Cited by 20 publications

References 14 publications

Investigating the mechanism of action of ginkgolides and bilobalide on absence seizures in maleWAG/Rij rats

Investigating the mechanism of action of ginkgolides and bilobalide on absence seizures in maleWAG/Rij rats

Progress in the Treatment of High Altitude Cerebral Edema: Targeting REDOX Homeostasis

The neuroprotective mechanisms of ginkgolides and bilobalide in cerebral ischemic injury: a literature review

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