WITHDRAWN: Sevoflurane post-conditioning protects primary rat cortical neurons against oxygen–glucose deprivation/resuscitation via down-regulation in mitochondrial apoptosis axis of Bid, Bim, Puma–Bax and Bak mediated by Erk1/2

Zhang, Limin; Xun, Zhao; Sun, Wenbo; Li, Rui; Jiang, Xiaojing

doi:10.1016/j.jns.2015.06.070

Cited by 23 publications

(12 citation statements)

References 28 publications

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“…While it has been shown that sevoflurane post‐conditioning can prevent the neuronal loss in the hippocampus, previous studies have demonstrated that sevoflurane post‐conditioning markedly reduces death of cortical neurons exposed to oxygen and glucose deprivation by increasing phosphorylation/activation of ERK1/2 (Zhang et al . ,b). Adding to this literature, this study was the first to show that activation of ERK1/2 in the hippocampus after repeated sevoflurane exposure following brain ischemia can prevent the subsequent development of PSD.…”

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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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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“…However, as we all know, the acting mechanisms of both intravenous anesthetic and inhaled anesthetic have not been clear so far (11). As for such a drug in the central nervous system, the safety deserves more attention when it facilitates surgical operation at the same time, especially the problem whether young children's neurological development is adversely affected, which is becoming urgent for medical workers to solve (11).…”

Section: Discussionmentioning

confidence: 99%

“…As for such a drug in the central nervous system, the safety deserves more attention when it facilitates surgical operation at the same time, especially the problem whether young children's neurological development is adversely affected, which is becoming urgent for medical workers to solve (11). More and more studies have gradually confirmed that there is a certain degree of neurotoxicity in sevoflurane and other inhaled anesthetics, which have significant impact on the development of children's cognitive abilities (12).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of vitexin reduces sevoflurane-induced neuronal apoptosis through HIF-1α, VEGF and p38 MAPK signaling pathway inï¿½vitro and in newborn rats

et al. 2018

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Abstract. Previous studies have demonstrated thatVitexin possesses antihypertensive, anti-inflammatory and potential anticancer effects. The present study aimed to investigate whether the protective effect of vitexin protects against sevoflurane-induced neuronal apoptosis and the underlying mechanisms of this protective effect. The results demonstrated that Vitexin pretreatment significantly reduced neuronal apoptosis, and inhibited caspase-3 activity, apoptosis regulator BAX protein expression and malondialdehyde levels in sevoflurane-induced newborn rats. In addition, Vitexin pretreatment increased superoxide dismutase and glutathione peroxidase activity. Furthermore, it was revealed that treatment with vitexin induced hypoxia inducible factor 1α subunit (HIF-1α) and vascular endothelial growth factor (VEGF) protein expression, and suppressed phosphorylated-p38 MAP kinase (p38) protein expression in sevoflurane-induced newborn rat. Together, the results of the current study suggest that the protective effect of vitexin reduces sevoflurane-induced neuronal apoptosis through HIF-1α-, VEGF-and p38-associated signaling pathways in newborn rats.

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“…It has been reported that Bim plays an important role in cell apoptosis (35)(36)(37). To investigate the potential role of Bim protein in the process of TAM-induced apoptosis, we further determined the Bim expression in TAM-sensitive MCF-7 cells (MCF-7) and TAM-resistant MCF-7 cells (MCF-7R) by Q-PCR and western blot analyses.…”

Section: Bim Is a Pro-apoptosis Effector Of Tam-induced Apoptosis In mentioning

confidence: 99%

GPER promotes tamoxifen-resistance in ER+ breast cancer cells by reduced Bim proteins through MAPK/Erk-TRIM2 signaling axis

Yin

Zhu

Liu

et al. 2017

International Journal of Oncology

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Tamoxifen resistance is a major clinical challenge in breast cancer treatment. Our previous studies find that GPER and its down-stream signaling play a pivotal role in the development of tamoxifen (TAM) resistance. cDNA array analysis indicated a set of genes associated with cell apoptosis are aberrant in GPER activated and TAM-resistant MCF-7R cells compared with TAM-sensitive MCF-7 cells. Among these genes, Bim (also named BCL2-L11), a member of the BH3-only pro-apoptotic protein family is significantly decreased, and TRIM RING ﬁnger protein TRIM2 (a ubiquitin ligase) is highly expressed in MCF-7R. To understand the mechanism of TAM-resistance in GPER activated ER+ breast cancer, the function of TRIM2 and Bim inducing cell apoptosis was studied. By using immunohistochemical and western blot analysis, there is an adverse correlation between TRIM2 and Bim in TAM-resistant breast tumor tissues and MCF-7R cells. Knockdown Bim in TAM-sensitive MCF-7 cells or overexpression of Bim in TAM-resistant MCF-7 cells significantly changed its sensibility to TAM through altering the levels of cleaved PARP and caspase-3. Activation of GPER and its downstream signaling MAPK/ERK, not PI3K/AKT, led to enhanced TRIM2 protein levels and affected the binding between TRIM2 and Bim which resulted in a reduced Bim in TAM-resistant breast cancer cells. Thus, the present study provides a novel insight to TAM-resistance in ER-positive breast cancer cells.

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WITHDRAWN: Sevoflurane post-conditioning protects primary rat cortical neurons against oxygen–glucose deprivation/resuscitation via down-regulation in mitochondrial apoptosis axis of Bid, Bim, Puma–Bax and Bak mediated by Erk1/2

Cited by 23 publications

References 28 publications

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

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

Protective effect of vitexin reduces sevoflurane-induced neuronal apoptosis through HIF-1α, VEGF and p38 MAPK signaling pathway inï¿½vitro and in newborn rats

GPER promotes tamoxifen-resistance in ER+ breast cancer cells by reduced Bim proteins through MAPK/Erk-TRIM2 signaling axis

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