Exendin-4 improved rat cortical neuron survival under oxygen/glucose deprivation through PKA pathway

Wang, M.-D.; Huang, Yan; Zhang, G.-P.; Mao, Ling; Xia, Yuanpeng; Mei, Yuan-wu; Hu, Bo

doi:10.1016/j.neuroscience.2012.09.025

Cited by 42 publications

(30 citation statements)

References 59 publications

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“…Exenatide was mainly used in those studies and neurons were protected against oxygen and glucose deprivation at least partly through the protein kinase A (PKA) pathway in vitro [9]. …”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Liraglutide for Stroke Model of Rats

Sato

Kameda

Yasuhara

et al. 2013

IJMS

110

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The number of diabetes mellitus (DM) patients is increasing, and stroke is deeply associated with DM. Recently, neuroprotective effects of glucagon-like peptide-1 (GLP-1) are reported. In this study, we explored whether liraglutide, a GLP-1 analogue exerts therapeutic effects on a rat stroke model. Wistar rats received occlusion of the middle cerebral artery for 90 min. At one hour after reperfusion, liraglutide or saline was administered intraperitoneally. Modified Bederson’s test was performed at 1 and 24 h and, subsequently, rats were euthanized for histological investigation. Peripheral blood was obtained for measurement of blood glucose level and evaluation of oxidative stress. Brain tissues were collected to evaluate the level of vascular endothelial growth factor (VEGF). The behavioral scores of liraglutide-treated rats were significantly better than those of control rats. Infarct volumes of liraglutide-treated rats at were reduced, compared with those of control rats. The level of derivatives of reactive oxygen metabolite was lower in liraglutide-treated rats. VEGF level of liraglutide-treated rats in the cortex, but not in the striatum significantly increased, compared to that of control rats. In conclusion, this is the first study to demonstrate neuroprotective effects of liraglutide on cerebral ischemia through anti-oxidative effects and VEGF upregulation.

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“…Exenatide was mainly used in those studies and neurons were protected against oxygen and glucose deprivation at least partly through the protein kinase A (PKA) pathway in vitro [9]. …”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Liraglutide for Stroke Model of Rats

Sato

Kameda

Yasuhara

et al. 2013

IJMS

110

View full text Add to dashboard Cite

show abstract

“…(iv) PD: augmenting dopaminergic cell survival, reducing neuroinflammation, increasing neurogenesis and improving motor coordination [118,150-152], which has recently translated to motor and cognitive improvements in moderately affected PD patients in an open label clinical trial [153]. (v) ALS: promoting motor neuron survival [122,154,155], (vi) Huntington's disease [119] and (vii) across a number of excitotoxic lesions models [114,155]. In defining cellular pathways mediating these neurotrophic/protective actions, thus far our studies implicate participation of PI3-kinase and ERK/MAPK dependent pathways, with additional involvement of protein kinase-A (PKA) signaling [72,121] to divert signaling away from apoptosis towards cell survival.…”

Section: Introduction: Traumatic Brain Injurymentioning

confidence: 99%

Incretin mimetics as pharmacologic tools to elucidate and as a new drug strategy to treat traumatic brain injury

Greig

Tweedie

Rachmany

et al. 2014

Alzheimer's & Dementia

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Traumatic brain injury (TBI), either as an isolated injury or in conjunction with other injuries, is an increasingly common occurring event. An estimated 1.7 million injuries occur within the US each year and 10 million people are affected annually worldwide. Indeed, some one-third (30.5%) of all injury-related deaths in the U.S. are associated with TBI, which will soon outstrip many common diseases as the major cause of death and disability. Associated with a high morbidity and mortality, and no specific therapeutic treatment, TBI has become a pressing public health and medical problem. The highest incidence of TBI occurs among young adults (15 to 24 years age) as well as in the elderly (75 years and older) who are particularly vulnerable as injury, often associated with falls, carries an increased mortality and worse functional outcome following lower initial injury severity. Added to this, a new and growing form of TBI, blast injury, associated with the detonation of improvised explosive devices in the war theaters of Iraq and Afghanistan, are inflicting a wave of unique casualties of immediate impact to both military personnel and civilians, for which long-term consequences remain unknown and may potentially be catastrophic. The neuropathology underpinning head injury is becoming increasingly better understood. Depending on severity, TBI induces immediate neuropathological effects that for the mildest form may be transient but with increasing severity cause cumulative neural damage and degeneration. Even with mild TBI, which represents the majority of cases, a broad spectrum of neurological deficits, including cognitive impairments, can manifest that may significantly influence quality of life. In addition, TBI can act as a conduit to longer-term neurodegenerative disorders. Prior studies of glucagon-like peptide-1 (GLP-1) and long-acting GLP-1 receptor agonists have demonstrated neurotrophic/neuroprotective activities across a broad spectrum of cellular and animal models of chronic neurodegenerative (Alzheimer's and Parkinson's diseases) and acute cerebrovascular (stroke) disorders. In line with the commonality in mechanisms underpinning these disorders as well as TBI, the current article reviews this literature and recent studies assessing GLP-1 receptor agonists as a potential treatment strategy for mild to moderate TBI.

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“…H89, a selective pharmacological PKA inhibitor, possesses the ability to suppress CREB phosphorylation in a concentration-dependent manner [12] and, thus, has been widely used as a laboratory agent in inhibition of CREB phosphorylation [13–17]. Recent studies have reported that H89 reduced the viability of primary cortical neurons [18]. In the present study, we thus used H89 to induce neural cell damage via downregulation of p-CREB [19,20] and investigated if Arc protects neural cells against CREB inactivation.…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effect of Arctigenin via Upregulation of P-CREB in Mouse Primary Neurons and Human SH-SY5Y Neuroblastoma Cells

Zhang

Wen

Ren

et al. 2013

IJMS

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Arctigenin (Arc) has been shown to act on scopolamine-induced memory deficit mice and to provide a neuroprotective effect on cultured cortical neurons from glutamate-induced neurodegeneration through mechanisms not completely defined. Here, we investigated the neuroprotective effect of Arc on H89-induced cell damage and its OPEN ACCESS Int. J. Mol. Sci. 2013, 1418658 potential mechanisms in mouse cortical neurons and human SH-SY5Y neuroblastoma cells. We found that Arc prevented cell viability loss induced by H89 in human SH-SY5Y cells. Moreover, Arc reduced intracellular beta amyloid (Aβ) production induced by H89 in neurons and human SH-SY5Y cells, and Arc also inhibited the presenilin 1(PS1) protein level in neurons. In addition, neural apoptosis in both types of cells, inhibition of neurite outgrowth in human SH-SY5Y cells and reduction of synaptic marker synaptophysin (SYN) expression in neurons were also observed after H89 exposure. All these effects induced by H89 were markedly reversed by Arc treatment. Arc also significantly attenuated downregulation of the phosphorylation of CREB (p-CREB) induced by H89, which may contribute to the neuroprotective effects of Arc. These results demonstrated that Arc exerted the ability to protect neurons and SH-SY5Y cells against H89-induced cell injury via upregulation of p-CREB.

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Exendin-4 improved rat cortical neuron survival under oxygen/glucose deprivation through PKA pathway

Cited by 42 publications

References 59 publications

Neuroprotective Effects of Liraglutide for Stroke Model of Rats

Neuroprotective Effects of Liraglutide for Stroke Model of Rats

Incretin mimetics as pharmacologic tools to elucidate and as a new drug strategy to treat traumatic brain injury

Neuroprotective Effect of Arctigenin via Upregulation of P-CREB in Mouse Primary Neurons and Human SH-SY5Y Neuroblastoma Cells

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