Xenon-delayed postconditioning attenuates spinal cord ischemia/reperfusion injury through activation AKT and ERK signaling pathways in rats

Liu, Shiyao; Yang, Yanwei; Jin, Mu; Hou, Siyu; Dong, Xian‐Zhe; Lu, Jiakai; Cheng, Weiping

doi:10.1016/j.jns.2016.07.009

Cited by 20 publications

(22 citation statements)

References 35 publications

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“…Both standard and modified distal posterior adaptation elicits neuroprotective effects against spinal cord ischemia by increasing expression of p-Akt and p-ERK 1/2 (Jiang et al, 2009). Xenon-delayed post-processing improves neurological function and attenuates SIRI in rats by increasing p-Akt and p-ERK 1/2 expression, and activating the Akt and ERK 1/2 signaling pathways (Liu et al, 2016b).…”

Section: The Extracellular Signal-regulated Kinase 1/2 Signaling Pathmentioning

confidence: 99%

Role of the Extracellular Signal-Regulated Kinase 1/2 Signaling Pathway in Ischemia-Reperfusion Injury

Kong

Liu

et al. 2019

Front. Physiol.

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Extracellular signal-regulated kinase 1/2 (ERK 1/2 ), an important member of the mitogen-activated protein kinase family, is found in many organisms, and it participates in intracellular signal transduction. Various stimuli induce phosphorylation of ERK 1/2 in vivo and in vitro . Phosphorylated ERK 1/2 moves to the nucleus, activates many transcription factors, regulates gene expression, and controls various physiological processes, finally inducing repair processes or cell death. With the aging of the population around the world, the occurrence of ischemia-reperfusion injury (IRI), especially in the brain, heart, kidney, and other important organs, is becoming increasingly serious. Abnormal activation of the ERK 1/2 signaling pathway is closely related to the development and the metabolic mechanisms of IRI. However, the effects of this signaling pathway and the underlying mechanism differ between various models of IRI. This review summarizes the ERK 1/2 signaling pathway and the molecular mechanism underlying its role in models of IRI in the brain, heart, liver, kidneys, and other organs. This information will help to deepen the understanding of ERK 1/2 signals and deepen the exploration of IRI treatment based on the ERK 1/2 study.

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Section: The Extracellular Signal-regulated Kinase 1/2 Signaling Pathmentioning

confidence: 99%

Role of the Extracellular Signal-Regulated Kinase 1/2 Signaling Pathway in Ischemia-Reperfusion Injury

Kong

Liu

et al. 2019

Front. Physiol.

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“…On studies of spinal cord ischemia, Jiang and colleagues (19) also demonstrated in their study that ischemic postconditioning preserved the motor function and intact motor neuron numbers of rabbits, and the mechanism was associated with enhanced expression of p‐Akt. Study by Liu et al (20) suggested the mechanism of xenon postconditioning against spinal cord I/R injury was partially induced by upregulation of Akt phosphorylation. The preliminary result of our study (5) suggested that SCS postconditioning, especially 2 Hz SCS postconditioning (when comparing with 50 Hz SCS postconditioning), effectively protected spinal cord from I/R injury on rabbits, which demonstrated as 2 Hz SCS preserved rabbits' hind limb neurological function and spinal cord motor neuron numbers and decreased the apoptosis rate of motor neurons.…”

Section: Discussionmentioning

confidence: 99%

The Neuroprotective Mechanism of Spinal Cord Stimulation in Spinal Cord Ischemia/Reperfusion Injury

Dong

Yang

et al. 2021

Neuromodulation: Technology at the Neural Interface

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“…The research on desflurane is limited; however, its protection against ischemia has been reported (Haelewyn et al, 2003). Xenon protects the brain against traumatic brain injury (TBI) (Harris et al, 2013) and ischemic injury (Dingley et al, 2006;Hobbs et al, 2008;Esencan et al, 2013;Sabir et al, 2014;Liu et al, 2016).…”

Section: Protective Effect Of Inhaled Anesthetic Gasesmentioning

confidence: 99%

“…Preconditioning has demonstrated protective effects against TBI (Harris et al, 2013;Deng et al, 2014;Khan et al, 2015;Shu et al, 2016), ischemic stroke (Dingley et al, 2006;Wang et al, 2011Wang et al, , 2016Yu et al, 2011;Liu et al, 2013;Shi et al, 2013), and hemorrhagic stroke (Gigante et al, 2011;Sheng et al, 2012). Post-conditioning is a relative new concept and it has been reported in ischemic stroke (Li et al, 2014;Yin et al, 2014;Lee et al, 2015;Liu et al, 2016).…”

Section: Protective Effect Of Inhaled Anesthetic Gasesmentioning

confidence: 99%

“…Both isoflurane and sevoflurane have been reported to activate phosphoinositide 3 kinase (PI3K) and protein kinase B (Akt) (Bickler and Fahlman, 2006;Ye et al, 2012;Zhang et al, 2014a), and sevoflurane can activate protein kinase C (Lee et al, 2015). Xenon may activate Nrf2 pathway by phosphorylating Akt and extracellular signal-regulated kinases (Liu et al, 2016).…”

Section: Anti-oxidative Mechanisms Of Inhaled Anesthetic Gasesmentioning

confidence: 99%

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Anti-oxidative aspect of inhaled anesthetic gases against acute brain injury

2016

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Acute brain injury is a critical and emergent condition in clinical settings, which needs to be addressed urgently. Commonly acute brain injuries include traumatic brain injury, ischemic and hemorrhagic strokes. Oxidative stress is a key contributor to the subsequent injuries and impedes the reparative process after acute brain injury; therefore, facilitating an anti-oxidative approach is important in the care of those diseases. Readiness to deliver and permeability to blood brain barrier are essential for the use of this purpose. Inhaled anesthetic gases are a group of such agents. In this article, we discuss the anti-oxidative roles of anesthetic gases against acute brain injury.

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Xenon-delayed postconditioning attenuates spinal cord ischemia/reperfusion injury through activation AKT and ERK signaling pathways in rats

Cited by 20 publications

References 35 publications

Role of the Extracellular Signal-Regulated Kinase 1/2 Signaling Pathway in Ischemia-Reperfusion Injury

Role of the Extracellular Signal-Regulated Kinase 1/2 Signaling Pathway in Ischemia-Reperfusion Injury

The Neuroprotective Mechanism of Spinal Cord Stimulation in Spinal Cord Ischemia/Reperfusion Injury

Anti-oxidative aspect of inhaled anesthetic gases against acute brain injury

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