Activation of cannabinoid receptor 1 is involved in protection against mitochondrial dysfunction and cerebral ischaemic tolerance induced by isoflurane preconditioning

Cai, Min; Yang, Qianzi; Li, G.; Sun, Sisi; Chen, Y.; Tian, Li; Dong, Hailong

doi:10.1093/bja/aex267

Cited by 13 publications

(6 citation statements)

References 46 publications

(19 reference statements)

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“…Consequently, administration of the chemical CypD inhibitors cyclosporine A (CsA) and gallic acid has been demonstrated to significantly diminish infarct size in vivo [85][86][87]. Additionally, isoflurane preconditioning has been reported to inhibit mPTP opening and elicit ischemic brain tolerance by activating cannabinoid receptor 1 (CB1R) [88]. The basic structure of the mPTP remains open to debate [89,90]; thus, further studies should be conducted to understand the molecular composition of the mPTP and to develop treatments targeting mPTP opening [90].…”

Section: Mitochondria and Cell Death In Ismentioning

confidence: 99%

Different Roles of Mitochondria in Cell Death and Inflammation: Focusing on Mitochondrial Quality Control in Ischemic Stroke and Reperfusion

et al. 2021

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Mitochondrial dysfunctions are among the main hallmarks of several brain diseases, including ischemic stroke. An insufficient supply of oxygen and glucose in brain cells, primarily neurons, triggers a cascade of events in which mitochondria are the leading characters. Mitochondrial calcium overload, reactive oxygen species (ROS) overproduction, mitochondrial permeability transition pore (mPTP) opening, and damage-associated molecular pattern (DAMP) release place mitochondria in the center of an intricate series of chance interactions. Depending on the degree to which mitochondria are affected, they promote different pathways, ranging from inflammatory response pathways to cell death pathways. In this review, we will explore the principal mitochondrial molecular mechanisms compromised during ischemic and reperfusion injury, and we will delineate potential neuroprotective strategies targeting mitochondrial dysfunction and mitochondrial homeostasis.

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Section: Mitochondria and Cell Death In Ismentioning

confidence: 99%

Different Roles of Mitochondria in Cell Death and Inflammation: Focusing on Mitochondrial Quality Control in Ischemic Stroke and Reperfusion

et al. 2021

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“…Isoflurane is a universally used inhaled anesthetic in the clinic. Some research has found isoflurane preconditioning (IP) can enhance tolerance of ischemia and play a protective role (17)(18)(19). Sun found IP supplied neuroprotection by directly regulating TLR4 expression, alleviating microglial activation, and neuroinflammation (20).…”

Section: Introductionmentioning

confidence: 99%

Isoflurane preconditioning effects on brain damage induced by electromagnetic pulse radiation through epigenetic modification of BDNF gene transcription

Tian¹,

Cai²,

Zhang³

et al. 2020

Ann Palliat Med

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Background: The effects of electromagnetic pulse (EMP) radiation on cognitive impairment have attracted much attention, but the mechanism is still unclear. Regulation of brain-derived neurotrophic factor (BDNF) gene expression has been found to promote memory formation and neuronal survival. Isoflurane preconditioning (IP) was reported to have a neuroprotective effect. In this study, we verified the protective effect of IP against brain injury induced by EMP exposure and examined the relation of this effect with BDNF gene regulation.Methods: Twenty-four hours before EMP exposure, rats were pretreated with 2% inhaled isoflurane for 30 minutes. At 24 hours after EMP injury, the Morris water maze test was carried out. Meanwhile, the other rats were executed and their brain tissues were used for Nissl staining, qRT-PCR, western blot and chromatin immunoprecipitation. Results:The Morris water maze results showed that 2% IP improved the spatial learning and memory ability of the rats. The Nissl staining results showed 2% of IP alleviated neuronal damage. Also, we detected the mRNA and protein expression of BDNF, and 2% IP significantly increased the expression of BDNF.We also found the expression level of histone deacetylase 2 (HDAC2) was increased and that EMP exposure significantly decreased H3 acetylation, while 2% IP reversed these phenomena, individually, BDNF transcription was activated, and neurogenesis after EMP exposure was alleviated.Conclusions: Our results suggested that 2% of IP alleviates cognitive impairment induced by EMP exposure in rats. Also, the sustained elevated level of BDNF gene transcription may be an essential mechanism for stimulating neurogenesis because of the increased level of HDAC2-dependent H3 acetylation.

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“…Many studies have shown that isoflurane has a protective effect on multiple organs in the model of ischemia-reperfusion injury [9–11]. The neuroprotective effect of isoflurane preconditioning has also been verified several times [12, 13], but its neuroprotective mechanism remains unclear. In the middle cerebral arterial occlusion (MCAO) model, isoflurane preconditioning achieves neuroprotective effects by inhibiting the activation of microglial cells and reducing the secretion of inflammatory factors [14].…”

Section: Introductionmentioning

confidence: 99%

Isoflurane Preconditioning Attenuates Brain Injury Induced by Electromagnetic Pulse via the TLR4/NFκB Signaling Pathway

Deng

Zhang³

et al. 2019

Oxidative Medicine and Cellular Longevity

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Electromagnetic pulse (EMP) is a unique type of electromagnetic radiation, and EMP exposure causes a series of biological effects. The nervous system is sensitive to EMP. We studied the neuroprotective effects of isoflurane preconditioning against EMP exposure and used hematoxylin-eosin staining (HE) to observe the effects of electromagnetic pulse and isoflurane preconditioning on neurons. Inflammatory cytokines were detected by enzyme-linked immunosorbent assay (ELISA). Western blotting was used to detect the expression of caspase-3, CD11b, TLR4, and NFκBp65. We found that after EMP exposure, the number of abnormal neurons had increased, and the expression of caspase-3, CD11b, TLR4, and NFκBp65 had also increased. Isoflurane preconditioning can reverse the above phenomenon. Moreover, we found that isoflurane preconditioning can reduce neuronal apoptosis and improve cognitive impairment induced by EMP. These findings indicate that isoflurane preconditioning can protect neurons in the cerebral cortex from EMP exposure, alleviate the inflammatory reaction and cell apoptosis, and improve cognitive impairment induced by EMP. These effects may occur through the downregulation of the TLR4/NFκB signaling pathway and the inhibition of microglial activation.

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Activation of cannabinoid receptor 1 is involved in protection against mitochondrial dysfunction and cerebral ischaemic tolerance induced by isoflurane preconditioning

Abstract: Our results indicate that IPC elicits brain ischaemic tolerance and mitochondrial protection by activating the CB1R, which provides a new mechanism for IPC-induced neuroprotection against cerebral ischaemia.

Cited by 13 publications

References 46 publications

Different Roles of Mitochondria in Cell Death and Inflammation: Focusing on Mitochondrial Quality Control in Ischemic Stroke and Reperfusion

Different Roles of Mitochondria in Cell Death and Inflammation: Focusing on Mitochondrial Quality Control in Ischemic Stroke and Reperfusion

Isoflurane preconditioning effects on brain damage induced by electromagnetic pulse radiation through epigenetic modification of BDNF gene transcription

Isoflurane Preconditioning Attenuates Brain Injury Induced by Electromagnetic Pulse via the TLR4/NFκB Signaling Pathway

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