Neuroprotection of Sevoflurane Against Ischemia/Reperfusion-Induced Brain Injury Through Inhibiting JNK3/Caspase-3 by Enhancing Akt Signaling Pathway

Wen, Xiangru; Fu, Yanyan; Liu, Hongzhi; Wu, Jian; Shao, Xiaoping; Zhang, Xun-Bao; Tang, Man; Shi, Yue; Ma, Kai; Zhang, Fang; Wang, Yiwen; Tang, Hui; Han, Dong; Zhang, Pu; Wang, Shuling; Xu, Zhaoyi; Song, Yuanjian

doi:10.1007/s12035-015-9111-8

Cited by 53 publications

(31 citation statements)

References 37 publications

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“…Caspase-3 is responsible for DNA fragmentation and plays a critical role in apoptosis (McIlwain et al, 2015; Sun et al, 2015). Recently, several researchers have suggested ischemia/reperfusion-induced brain injury might be ameliorated by inhibiting caspase-3 signaling (Wen et al, 2016;Yang et al, 2015a), and in the present study, glycyrrhizinwas found to inhibit increase in caspase-3 and -9 levelscaused by MCAO-induced brain damage (Figure 4).…”

Section: Discussionsupporting

confidence: 66%

Effects of Glycyrrhizin Pre-Treatment on Transient Ischemic Brain Injury in Mice

Lim¹,

Lim²,

Lee³

et al. 2017

Afr J Tradit Complement Altern Med

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Background: Ischemia-induced brain damage is the leading cause of adult disability and the fifth leading cause of death, and thus, the development of anti-apoptotic neuro-protective therapeutic agents is viewed as an attractive developmental strategy. Glycyrrhizin is the main sweet component in licorice and has a number of pharmacological activities, which include neuro-protective, anti-fungal, and anti-cariogenic activities. This study was undertaken to investigate the effects of glycyrrhizin on ischemia-induced brain damage. Materials and Methods: In infarct volumes and the levels of several apoptosis-related proteins, caspase-3, -8, 9, Bcl-xL, Bcl-2,and their activities in the brains of middle cerebral artery occlusion (MCAO) treated mice were measured using western blotting methods. Results: Single pre-treatment with glycyrrhizin (10-100 mg/kg)at 2 hours before MCAO significantly reduced infarct volumes at 24h after MCAO. In addition, glycyrrhizin effectively inhibited the activations of caspase-3 and -9 and the down-regulation of Bcl-xLprotein caused by MCAO. Conclusion:The neuro-protective effect of glycyrrhizin was found to be due to its regulation of apoptosisrelated proteins signals.The authors suggest glycyrrhizin be considered a potential candidate for the treatment of ischemia induced brain damage.

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Section: Discussionsupporting

confidence: 66%

Effects of Glycyrrhizin Pre-Treatment on Transient Ischemic Brain Injury in Mice

Lim¹,

Lim²,

Lee³

et al. 2017

Afr J Tradit Complement Altern Med

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“…Relatively loose association of HS with the endothelial glycocalyx likely contributes to the limited protective effect of sevoflurane on the shedding of HS at the beginning of the reperfusion. [11][12][13][14][15][16]18,29 Conversely, Syn-1 has a solid association with the endothelial glycocalyx. As a result, the peak of the Syn-1 release appeared much later during reperfusion.…”

Section: Discussionmentioning

confidence: 99%

“…8 Previous studies have demonstrated that sevoflurane, a volatile anesthetic, can protect various organs or tissues against ischemia-reperfusion injury, including the brain, heart, intestine, and lung, in both humans and laboratory animals. [9][10][11][12][13][14] Furthermore, sevoflurane can preserve the endothelial glycocalyx against ischemia-reperfusion injury in heart tissue. 10 Some studies examined the effects of sevoflurane pretreatment on hepatic tissues following the ischemia-reperfusion injury.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of sevoflurane in hepatic ischemia-reperfusion injury

Yuan

Zhao

et al. 2016

Int J Immunopathol Pharmacol

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The endothelial glycocalyx plays a critical role in the regulation of vascular structure and functions. Previous studies have demonstrated that sevoflurane, a volatile anesthetic, can preserve the endothelial glycocalyx in heart tissues against ischemia-reperfusion injury. However, little is known about the effects of sevoflurane pretreatment on the vascular structure and functions of liver tissues following ischemia-reperfusion injury. To this end, female Sprague-Dawley rats (n = 28) were anesthetized either with ketamine (80-120 mg/kg, i.p.) or with one minimum alveolar concentration (MAC) sevoflurane (2% v/v). Following in vivo hepatic ischemia procedure, the liver was isolated and reperfusion was produced. During the period of reperfusion, liver reperfusion samples were collected, and the concentrations of heparan sulfate and syndecan-1 (Syn-1), and the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) enzymes, were measured. The morphology of hepatocytes and endothelial glycocalyx were then assessed by using the light and electron microscopies, respectively. Ischemia-reperfusion increased the release of HS and Syn-1, and elevated the levels of ALT and AST in a time-dependent manner. However, sevoflurane pretreatment reduced the release of HS and Syn-1and attenuated the levels of ALT and AST, in a time-dependent manner, as compared with ketamine pretreatment. Furthermore, sevoflurane pretreatment decreased the shedding of endothelial glycocalyx and hepatocytes necrosis. Sevoflurane pretreatment preserved the endothelial glycocalyx in the liver tissue against ischemia-reperfusion injury. The effect appears to help protect hepatocytes against ischemia-reperfusion-induced necrosis.

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“…Specifically, sevoflurane post‐conditioning can significantly improve the long‐term cognitive performance of the rats, increase the number of surviving neurons in cornus ammonis (CA)1 and CA3 hippocampal regions, and protect the histomorphology of the hippocampus (Wen et al . ; Lai et al . ).…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane prevents stroke‐induced depressive and anxiety behaviors by promoting cannabinoid receptor subtype I‐dependent interaction between β‐arrestin 2 and extracellular signal‐regulated kinases 1/2 in the rat hippocampus

Zhang

Sun³

et al. 2016

Journal of Neurochemistry

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One of the most frequent psychological consequences of stroke is depression. Previous animal studies have demonstrated that post-conditioning with sevoflurane protects against focal cerebral ischemia and reperfusion injury. Thus, we hypothesized that repeated exposure to sevoflurane after transient ischemia can prevent the development of depressive-like behavior. To test this hypothesis, we induced transient cerebral ischemia via transient occlusion of bilateral common carotid arteries and examined the effects of subsequent repeated exposure to sevoflurane on sucrose preference, locomotor activity, and rearing activity in rats. To explore the putative neurobiological mechanisms, we further investigated the roles of hippocampal CB1 receptor in the behavioral effects of sevoflurane. We found that repeated sevoflurane exposures reversed ischemia-induced depressivelike behaviors. Furthermore, CB1 receptor inhibition in the dorsal hippocampus (DH) abolished the effects of sevoflurane exposures on ischemia-induced depressive-like behaviors.In addition, repeated sevoflurane exposures increased CB1 receptor expression and endocannabinoids levels in the DH of ischemic rats. Moreover, repeated sevoflurane exposures enhanced the expression of b-arrestin 2, increased the activation of extracellular signal-regulated kinases (ERK)1/2, and promoted the interaction of b-arrestin 2 and ERK1/2 in the DH, and such effects were reversed by CB1 receptor antagonism in the DH. Finally, b-arrestin 2 expression and ERK1/2 activation in the DH were critical for the preventative effects of sevoflurane exposures on ischemia-induced depressive-like behaviors. Taken together, our results suggested that sevoflurane exposure after brain ischemia may prevent the development of depression, and such preventative effects of sevoflurane are likely ascribed to the activation of CB1 receptor-mediated b-arrestin 2-ERK1/2 signaling pathways.

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Neuroprotection of Sevoflurane Against Ischemia/Reperfusion-Induced Brain Injury Through Inhibiting JNK3/Caspase-3 by Enhancing Akt Signaling Pathway

Cited by 53 publications

References 37 publications

Effects of Glycyrrhizin Pre-Treatment on Transient Ischemic Brain Injury in Mice

Effects of Glycyrrhizin Pre-Treatment on Transient Ischemic Brain Injury in Mice

Protective effects of sevoflurane in hepatic ischemia-reperfusion injury

Sevoflurane prevents stroke‐induced depressive and anxiety behaviors by promoting cannabinoid receptor subtype I‐dependent interaction between β‐arrestin 2 and extracellular signal‐regulated kinases 1/2 in the rat hippocampus

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