Effects of Physical Activity and Ginkgo Biloba on Cognitive Function and Oxidative Stress Modulation in Ischemic Rats

Vaghef, Ladan; Gharamaleki, Hassan Bafandeh

doi:10.1055/s-0036-1588024

Cited by 5 publications

(2 citation statements)

References 51 publications

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“…On the contrary, GBE that has different beneficial ingredients for mental health showed amelioration in detrimental effect of chronic HH exposure on spatial memory. Similar observations were reported previously by Vaghef et al (2017) which illustrated protective effects of Ginkgo biloba L. on oxidative stress as well as memory impairments induced by transient cerebral ischemia. GBE has been reported to exhibit anti-inflammatory and neuroprotective properties in other studies ( Liang et al, 2018 ).…”

Section: Discussionsupporting

confidence: 92%

Ginkgo biloba L. Prevents Hypobaric Hypoxia–Induced Spatial Memory Deficit Through Small Conductance Calcium-Activated Potassium Channel Inhibition: The Role of ERK/CaMKII/CREB Signaling

et al. 2021

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Hypobaric hypoxia (HH) is a stressful condition, which is more common at high altitudes and can impair cognitive functions. Ginkgo biloba L. leaf extract (GBE) is widely used as herbal medicine against different disorders. Its ability to improve cognitive functions, reduce oxidative stress, and promote cell survival makes it a putative therapeutic candidate against HH. The present study has been designed to explore the effect of GBE on HH-induced neurodegeneration and memory impairment as well as possible signaling mechanisms involved. 220–250 gm (approximately 6- to 8-week-old) Sprague Dawley rats were randomly divided into different groups. GBE was orally administered to respective groups at a dose of 100 mg/kg/day throughout the HH exposure, i.e., 14 days. Memory testing was performed followed by hippocampus isolation for further processing of different molecular and morphological parameters related to cognition. The results indicated that GBE ameliorates HH-induced memory impairment and oxidative damage and reduces apoptosis. Moreover, GBE modulates the activity of the small conductance calcium-activated potassium channels, which further reduces glutamate excitotoxicity and apoptosis. The exploration of the downstream signaling pathway demonstrated that GBE administration prevents HH-induced small conductance calcium-activated potassium channel activation, and that initiates pro-survival machinery by activating extracellular signal–regulated kinase (ERK)/calmodulin-dependent protein kinase II (CaMKII) and the cAMP response element–binding protein (CREB) signaling pathway. In summary, the current study demonstrates the beneficial effect of GBE on conditions like HH and provides various therapeutic targets involved in the mechanism of action of GBE-mediated neuroprotection.

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Section: Discussionsupporting

confidence: 92%

Ginkgo biloba L. Prevents Hypobaric Hypoxia–Induced Spatial Memory Deficit Through Small Conductance Calcium-Activated Potassium Channel Inhibition: The Role of ERK/CaMKII/CREB Signaling

et al. 2021

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“…Pre-treatment and post-treatment with EGB1212 increased both hippocampal neuron survival and spatial learning and memory functions after global cerebral ischemia/reperfusion in rats (Yin et al 2013). However, Vaghef and Bafandeh Gharamaleki (2017) reported that pretreatment with G. biloba was not as effective as exercise in recovering from memory impairment, although its effect on oxidative stress in the hippocampus was supported. Moreover, GK alleviated neurological impairments and accelerated angiogenesis of the ipsilateral cortex and striatum injured by tMCAO in a mouse model (Chen et al 2018c).…”

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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Endurance training on rodent brain antioxidant capacity: A meta-analysis

Souza

Moraes

Augusto

et al. 2019

Neuroscience Research

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Effects of Physical Activity and Ginkgo Biloba on Cognitive Function and Oxidative Stress Modulation in Ischemic Rats

Cited by 5 publications

References 51 publications

Ginkgo biloba L. Prevents Hypobaric Hypoxia–Induced Spatial Memory Deficit Through Small Conductance Calcium-Activated Potassium Channel Inhibition: The Role of ERK/CaMKII/CREB Signaling

Ginkgo biloba L. Prevents Hypobaric Hypoxia–Induced Spatial Memory Deficit Through Small Conductance Calcium-Activated Potassium Channel Inhibition: The Role of ERK/CaMKII/CREB Signaling

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

Endurance training on rodent brain antioxidant capacity: A meta-analysis

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