Isoflurane reduces pain and inhibits apoptosis of myocardial cells through the phosphoinositide 3-kinase/protein kinaseï¿½B signaling pathway in mice during cardiac surgery

Pi, Zhibing; Lin, Hai; Yang, Jianping

doi:10.3892/mmr.2018.8642

Cited by 7 publications

(5 citation statements)

References 42 publications

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“…To further test this idea, we injected NMDA into eyes of Thy1-GFP mice, in which most, if not all, RGCs are GFP-expressing, and labeled NMDA-treated retinas using an anti-CASP3 antibody to identify cells undergoing apoptosis ( Pi et al, 2018 ). The results show that some GFP-positive cells are also CASP3-positive 3 h after NMDA injection ( Figure 2H ), indicating that RGCs actively undergoing apoptosis are still GFP positive, while no CASP3-positive RGCs are found in non-injected eyes (data not shown).…”

Section: Resultsmentioning

confidence: 99%

The Susceptibility of Retinal Ganglion Cells to Glutamatergic Excitotoxicity Is Type-Specific

et al. 2019

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Retinal ganglion cells (RGCs) are the only output neurons that conduct visual signals from the eyes to the brain. RGC degeneration occurs in many retinal diseases leading to blindness and increasing evidence suggests that RGCs are susceptible to various injuries in a type-specific manner. Glutamate excitotoxicity is the pathological process by which neurons are damaged and killed by excessive stimulation of glutamate receptors and it plays a central role in the death of neurons in many CNS and retinal diseases. The purpose of this study is to characterize the susceptibility of genetically identified RGC types to the excitotoxicity induced by N-methyl-D-aspartate (NMDA). We show that the susceptibility of different types of RGCs to NMDA excitotoxicity varies significantly, in which the αRGCs are the most resistant type of RGCs to NMDA excitotoxicity while the J-RGCs are the most sensitive cells to NMDA excitotoxicity. These results strongly suggest that the differences in the genetic background of RGC types might provide valuable insights for understanding the selective susceptibility of RGCs to pathological insults and the development of a strategy to protect RGCs from death in disease conditions. In addition, our results show that RGCs lose dendrites before death and the sequence of the morphological and molecular events during RGC death suggests that the initial insult of NMDA excitotoxicity might set off a cascade of events independent of the primary insults. However, the kinetics of dendritic retraction in RGCs does not directly correlate to the susceptibility of type-specific RGC death.

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Section: Resultsmentioning

confidence: 99%

The Susceptibility of Retinal Ganglion Cells to Glutamatergic Excitotoxicity Is Type-Specific

et al. 2019

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“…Isoflurane, a general inhalation anesthetic used for the induction and maintenance of general anesthesia, promotes PI3K/AKT activation, upregulates B-cell lymphoma 2 (Bcl-2)-associated X protein Bcl-2 expression levels, and reduces the expression levels of caspase 3 and caspase 8 in myocardial cells. Isoflurane is beneficial for pain attenuation and inhibits apoptosis in myocardial cells via the PI3K/AKT signaling pathway in mice during cardiac surgery [ 132 ]. Further, Masahiko Kawaguchi et al (2004) showed that isoflurane reduced the early development of neuronal apoptosis in rats subjected to focal cerebral ischemia [ 133 ].…”

Section: Apoptosis and Clinical Implicationsmentioning

confidence: 99%

Apoptosis and (in) Pain—Potential Clinical Implications

et al. 2022

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The deregulation of apoptosis is involved in the development of several pathologies, and recent evidence suggests that apoptosis may be involved in chronic pain, namely in neuropathic pain. Neuropathic pain is a chronic pain state caused by primary damage or dysfunction of the nervous system; however, the details of the molecular mechanisms have not yet been fully elucidated. Recently, it was found that nerve endings contain transient receptor potential (TRP) channels that sense and detect signals released by injured tissues and respond to these damage signals. TRP channels are similar to the voltage-gated potassium channels or nucleotide-gated channels that participate in calcium and magnesium homeostasis. TRP channels allowing calcium to penetrate into nerve terminals can activate apoptosis, leading to nerve terminal destruction. Further, some TRPs are activated by acid and reactive oxygen species (ROS). ROS are mainly produced in the mitochondrial respiratory chain, and an increase in ROS production and/or a decrease in the antioxidant network may induce oxidative stress (OS). Depending on the OS levels, they can promote cellular proliferation and/or cell degeneration or death. Previous studies have indicated that proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α), play an important role in the peripheral mediation of neuropathic pain. This article aims to perform a review of the involvement of apoptosis in pain, particularly the role of OS and neuroinflammation, and the clinical relevance of this knowledge. The potential discovery of new biomarkers and therapeutic targets can result in the development of more effective and targeted drugs to treat chronic pain, namely neuropathic pain. Highlights: Oxidative stress and neuroinflammation can activate cell signaling pathways that can lead to nerve terminal destruction by apoptosis. These could constitute potential new pain biomarkers and targets for therapy in neuropathic pain.

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“…Although anesthetics are widely used during a range of procedures, their exact mechanism, and overall outcomes are still not completely understood. Some studies have suggested that isoflurane has some anti-cell death properties [41][42][43]. Ketamine is reported to reduce brain injury by inhibiting apoptosis [11,44,45] and exerting anti-inflammatory effects [6,46].…”

Section: Discussionmentioning

confidence: 99%

Distinctive effect of anesthetics on the effect of limb remote ischemic postconditioning following ischemic stroke

et al. 2020

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Limb remote ischemic postconditioning (LRIP) has been reported as an effective method to reduce the induced experimental stroke damage after ischemic reperfusion (IR) injury. Studies suggest that anesthetics used during induction of ischemic stroke can reduce IR injury, which could affect the actual mechanisms of neuroprotection by LRIP. This study focuses on the comparative effects of anesthetics such as isoflurane and ketamine-xylazine on ischemic injury when used during LRIP. Adult C57BL/6 mice were anesthetized by isoflurane or halothane, and transient middle cerebral artery occlusion (MCAO) was induced through insertion of the filament. Under isoflurane or ketamine-xylazine anesthesia, LRIP was performed after 90 min of reperfusion by carrying out three cycles of 5 min ischemia/5 min reperfusion of the bilateral hind limbs for one session per day for a total of 3 days. Results showed that the use of different anesthetics-isoflurane or ketamine-xylazine-during LRIP had no effects on body weight. However, LRIP was able to improve neurological function as observed by the neurological deficit score in ischemic mice. Interestingly, the neurological deficit in the group where ketamine-xylazine was used was better than the group where isoflurane was used during LRIP. Furthermore, the LRIP was able to prolong the period of the ischemic mice on the rotarod and this effect was more significant in the groups where ketamine-xylazine was used during LRIP. Moreover, LRIP significantly attenuated the infarction volume; however, this effect was independent of the anesthetic used during LRIP. From these results, we conclude that ischemic mice that were subjected to LRIP under ketamine-xylazine anesthesia had better neurological deficit outcomes after stroke.

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Isoflurane reduces pain and inhibits apoptosis of myocardial cells through the phosphoinositide 3-kinase/protein kinaseï¿½B signaling pathway in mice during cardiac surgery

Cited by 7 publications

References 42 publications

The Susceptibility of Retinal Ganglion Cells to Glutamatergic Excitotoxicity Is Type-Specific

The Susceptibility of Retinal Ganglion Cells to Glutamatergic Excitotoxicity Is Type-Specific

Apoptosis and (in) Pain—Potential Clinical Implications

Distinctive effect of anesthetics on the effect of limb remote ischemic postconditioning following ischemic stroke

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