Effects of dexmedetomidine on the release of glial cell line-derived neurotrophic factor from rat astrocyte cells

Yan, Min; Dai, Haibin; Ding, Tingting; Dai, An-lu; Zhang, Fengjiang; Lu, Yu; Chen, Gang; Chen, Zhong

doi:10.1016/j.neuint.2011.01.013

Cited by 44 publications

(38 citation statements)

References 31 publications

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“…However, few of these clinical trials succeeded due to the occurrence of severe sided effects [33–36]. In conclusion, the current study supported that astroglia were indispensable for the modulation of the survival and the function of DA neurons and provided a new therapeutic potential targeting astroglia for PD treatment.…”

Section: Discussionsupporting

confidence: 68%

Resveratrol Produces Neurotrophic Effects on Cultured Dopaminergic Neurons through Prompting Astroglial BDNF and GDNF Release

Zhang

Wang

Liu

et al. 2012

Evidence-Based Complementary and Alternative Medicine

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Increasing evidence indicated astroglia-derived neurotrophic factors generation might hold a promising therapy for Parkinson's disease (PD). Resveratrol, naturally present in red wine and grapes with potential benefit for health, is well known to possess a number of pharmacological activities. Besides the antineuroinflammatory properties, we hypothesized the neuroprotective potency of resveratrol is partially due to its additional neurotrophic effects. Here, primary rat midbrain neuron-glia cultures were applied to investigate the neurotrophic effects mediated by resveratrol on dopamine (DA) neurons and further explore the role of neurotrophic factors in its actions. Results showed resveratrol produced neurotrophic effects on cultured DA neurons. Additionally, astroglia-derived neurotrophic factors release was responsible for resveratrol-mediated neurotrophic properties as evidenced by the following observations: (1) resveratrol failed to exert neurotrophic effects on DA neurons in the cultures without astroglia; (2) the astroglia-conditioned medium prepared from astroglia-enriched cultures treated with resveratrol produced neurotrophic effects in neuron-enriched cultures; (3) resveratrol increased neurotrophic factors release in the concentration- and time-dependent manners; (4) resveratrol-mediated neurotrophic effects were suppressed by blocking the action of the neurotrophic factors. Together, resveratrol could produce neurotrophic effects on DA neurons through prompting neurotrophic factors release, and these effects might open new alternative avenues for neurotrophic factor-based therapy targeting PD.

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Section: Discussionsupporting

confidence: 68%

Resveratrol Produces Neurotrophic Effects on Cultured Dopaminergic Neurons through Prompting Astroglial BDNF and GDNF Release

Zhang

Wang

Liu

et al. 2012

Evidence-Based Complementary and Alternative Medicine

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“…Yan et al [2011] reported that dexmedetomidine promotes the release of glial cell-derived neurotrophic factor from astrocytes to protect neurons after stroke through activation of protein kinase Cα and cAMP response element-binding protein. Degos et al [2013] explained this effect by the ability of dexmedetomidine to increase the expression of astrocytic brain-derived neurotrophic factor, which acts directly on astrocyte α 2 -adrenergic receptors leading to phosphorylation of extracellular signal-regulated kinase.…”

Section: Discussionmentioning

confidence: 99%

Reactive Astrogliosis in an Experimental Model of Fibromyalgia: Effect of Dexmedetomidine

Abd-ellatief

Mohamed

Kotb

2018

Cells Tissues Organs

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To our knowledge, this is the first study which investigates the induction of neuroinflammation in rats using an acidic-saline model of fibromyalgia. It is well known that the hippocampus has a fundamental role in pain perception, and astrocytes play a crucial role in pain signaling. Our aim is to evaluate the ability of dexmedetomidine to attenuate the inflammatory responses induced in astrocytes. In a group of healthy rats, induction of chronic muscle pain by intramuscular injection of 100 µL of acidic saline on days 0 and 5 resulted in peripheral sensitization (measured using the von Frey test) and significant (p < 0.05) increases in IL-1β (160.2 ± 1.1 to 335.2 ± 1.8), IL-6 (100.1 ± 1.4 to 202.4 ± 1.1), and TNF-α (60.0 ± 0.7 to 115.5 ± 1). Light and electron microscopy revealed degenerative changes in the hippocampus and reactive astrogliosis. Immunohistochemistry showed increased expression of glial fibrillary acid protein and inducible nitric oxide synthase. Surprisingly, treatment with a single dose of an α₂-adrenergic agonist, dexmedetomidine (5 µg/kg i.p.), attenuated these changes. This trial suggests that dexmedetomidine possibly directly acts on astrocytes, and a peripheral action is also suggested.

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“…Western blots were performed as previously described [30]. The rabbits’ spinal cords were homogenized, and total proteins were purified using cell and tissue protein extraction reagents according to manufacturer’s instructions (KC-415; KangChen, Shanghai, China).…”

Section: Methodsmentioning

confidence: 99%

Ischemic Preconditioning Protects against Spinal Cord Ischemia-Reperfusion Injury in Rabbits by Attenuating Blood Spinal Cord Barrier Disruption

Fang

Sun

et al. 2013

IJMS

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Ischemic preconditioning has been reported to protect against spinal cord ischemia-reperfusion (I-R) injury, but the underlying mechanisms are not fully understood. To investigate this, Japanese white rabbits underwent I-R (30 min aortic occlusion followed by reperfusion), ischemic preconditioning (three cycles of 5 min aortic occlusion plus 5 min reperfusion) followed by I-R, or sham surgery. At 4 and 24 h following reperfusion, neurological function was assessed using Tarlov scores, blood spinal cord barrier permeability was measured by Evan’s Blue extravasation, spinal cord edema was evaluated using the wet-dry method, and spinal cord expression of zonula occluden-1 (ZO-1), matrix metalloproteinase-9 (MMP-9), and tumor necrosis factor-α (TNF-α) were measured by Western blot and a real-time polymerase chain reaction. ZO-1 was also assessed using immunofluorescence. Spinal cord I-R injury reduced neurologic scores, and ischemic preconditioning treatment ameliorated this effect. Ischemic preconditioning inhibited I-R-induced increases in blood spinal cord barrier permeability and water content, increased ZO-1 mRNA and protein expression, and reduced MMP-9 and TNF-α mRNA and protein expression. These findings suggest that ischemic preconditioning attenuates the increase in blood spinal cord barrier permeability due to spinal cord I-R injury by preservation of tight junction protein ZO-1 and reducing MMP-9 and TNF-α expression.

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Effects of dexmedetomidine on the release of glial cell line-derived neurotrophic factor from rat astrocyte cells

Cited by 44 publications

References 31 publications

Resveratrol Produces Neurotrophic Effects on Cultured Dopaminergic Neurons through Prompting Astroglial BDNF and GDNF Release

Resveratrol Produces Neurotrophic Effects on Cultured Dopaminergic Neurons through Prompting Astroglial BDNF and GDNF Release

Reactive Astrogliosis in an Experimental Model of Fibromyalgia: Effect of Dexmedetomidine

Ischemic Preconditioning Protects against Spinal Cord Ischemia-Reperfusion Injury in Rabbits by Attenuating Blood Spinal Cord Barrier Disruption

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