Isoflurano fornece neuroproteção em lesão cerebral hipóxico‐isquêmica neonatal por inibição da apoptose

Zhao, Dean; Bi, Lingyun; Huang, Qian; Zhang, Fang‐Min; Zi-ming, Han

doi:10.1016/j.bjan.2016.08.003

Cited by 14 publications

(6 citation statements)

References 37 publications

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“…8 At present, mild hypothermia therapy is commonly used to treat HIE in clinical practice, but 40%-50% of children with severe HIE still develop serious sequelae after treatment. 9 Isoflurane (ISO) is an inhalation anesthetic that inhibits inflammation, prevents oxidative stress, and has some neuroprotective effects. 10 After many years of clinical application, it has been found that it has the characteristics of reducing intracranial pressure, reducing cerebral oxygen consumption, inducing and maintaining balance, promoting rapid recovery, and inducing few side effects.…”

Section: Introductionmentioning

confidence: 99%

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Protective effect of isoflurane preconditioning on neurological function in rats with HIE

Fei‐Sun

Huang

Qin

et al. 2022

Ibrain

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Hypoxic ischemic encephalopathy (HIE) is an important cause of neonatal death and disability, which can lead to long-term neurological and motor dysfunction. At present, the treatment mainly focuses on the symptomatic treatment in the acute phase and rehabilitation after injury, but the effect is not satisfactory, and more effective methods are urgently needed. Due to the widespread use of inhalation anesthetics in surgery, it has been found that iso urane (ISO) preconditioning may have a positive effect on neuroprotection. The aim of this study was to investigate the effects of ISO preconditioning on neurological function and behavior in HIE rats. MethodsNeonatal rats were used to create hypoxic-ischemic (HI) model by ligating the right common carotid artery at 7 days and then in a hypoxia chamber. The effects of anesthetic drugs on neurological function after one hour of ISO preconditioning were assessed after modeling by Morris water maze(MWM), Ymaze, and rotarod tests at one month. Thereafter, samples were taken at 1 and 42 days for Nissl staining and Hematoxylin-Eosin (HE) staining to observe neuronal number and histomorphology changes. The relationship of behaviour and morphology tests were measured. ResultsIschemia and hypoxia could induce neuronal injury, neurological dysfunction and severe long-term motor function injury. Histological staining and behavioural evaluations were performed to elucidate the pathological changes and neurobehavioural variation after ISO treatment. We found ISO administration signi cantly reduced the infarct volume of brain tissues and improved the autonomous activities of neonatal rats, ISO preconditioning signi cantly reduced neuronal apoptosis induced by HI, reduced cerebral infarction volume, improved histopathological damage of nerve cells, improved long-term cognitive function, and attenuated HI-induced Nissl total cells to reduce and reduce long-term spatial memory impairment caused by hypoxia-ischemia during the maturation of injured brain. ConclusionISO preconditioning can protect the brain injury and promote the recovery of neurological function in neonatal rats with HIE, which may be through inhibiting the neuronal cell death in the cortex and hippocampus after HI.

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Section: Introductionmentioning

confidence: 99%

“…Herein, an unsolved medical problem needs to be studied to elucidate the mechanism and find effective neurotherapeutic goals 8 . At present, mild hypothermia therapy is commonly used to treat HIE in clinical practice, but 40%–50% of children with severe HIE still develop serious sequelae after treatment 9 …”

Section: Introductionmentioning

confidence: 99%

Protective effect of isoflurane preconditioning on neurological function in rats with HIE

Fei‐Sun

Huang

Qin

et al. 2022

Ibrain

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“…Isoflurane is a common volatile anesthetic in the clinic and protects against ischemic brain injury [129] by suppressing apoptosis [130]. Preconditioning using a clinically relevant concentration of isoflurane can attenuate renal IRI.…”

Section: Other Anesthetics In Irimentioning

confidence: 99%

Opioids Preconditioning Upon Renal Function and Ischemia-Reperfusion Injury: A Narrative Review

et al. 2019

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Kidneys have an important role in regulating water volume, blood pressure, secretion of hormones and acid-base and electrolyte balance. Kidney dysfunction derived from acute injury can, under certain conditions, progress to chronic kidney disease. In the late stages of kidney disease, treatment is limited to replacement therapy: Dialysis and transplantation. After renal transplant, grafts suffer from activation of immune cells and generation of oxidant molecules. Anesthetic preconditioning has emerged as a promising strategy to ameliorate ischemia reperfusion injury. This review compiles some significant aspects of renal physiology and discusses current understanding of the effects of anesthetic preconditioning upon renal function and ischemia reperfusion injury, focusing on opioids and its properties ameliorating renal injury. According to the available evidence, opioid preconditioning appears to reduce inflammation and reactive oxygen species generation after ischemia reperfusion. Therefore, opioid preconditioning represents a promising strategy to reduce renal ischemia reperfusion injury and, its application on current clinical practice could be beneficial in events such as acute renal injury and kidney transplantation.

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“…Isoflurane (ISO) is a common volatile anesthetic in the clinic and protects against ischemic brain injury (Cheon et al, 2017). For example, isoflurane provides neuroprotection in ischemic brain injury by suppressing apoptosis (Zhao et al, 2016). ISO post-conditioning can ameliorate intracranial hemorrhage and infarction volume in tPA-exaggerated brain injury (Kim et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

TGF-β2 Induces Gli1 in a Smad3-Dependent Manner Against Cerebral Ischemia/Reperfusion Injury After Isoflurane Post-conditioning in Rats

Yang

Yin

et al. 2019

Front. Neurosci.

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Isoflurane (ISO) post-conditioning attenuates cerebral ischemia/reperfusion (I/R) injury, but the underlying mechanism is incompletely elucidated. Transforming growth factor beta (TGF-β) and hedgehog (Hh) signaling pathways govern a wide range of mechanisms in the central nervous system. We aimed to investigate the effect of the TGF-β2/Smad3 and sonic hedgehog (Shh)/Glioblastoma (Gli) signaling pathway and their crosstalk in the hippocampus of rats with ISO post-conditioning after cerebral I/R injury. Adult male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO), 1.5 h occlusion and 24 h reperfusion (MCAO/R). To assess the effect of ISO after I/R injury, various approaches were used, including neurobehavioral tests, TTC staining, HE staining, Nissl staining, TUNEL staining, immunofluorescence (IF), qRT-PCR (quantitative real-time polymerase chain reaction) and Western blot. The ISO post-conditioning group (ISO group) received 1 h ISO post-conditioning when reperfusion was initiated, leading to lower infarct volumes and neurologic deficit scores, more surviving neurons, and less damaged and apoptotic neurons. IF staining, qRT-PCR and Western blot showed high expression levels of TGF-β2, Shh and Gli1 in the hippocampal CA1 of the ISO group. Phosphorylated Smad3 (p-Smad3), Patched (Ptch), and Smoothed (Smo) were also increased at protein level in the ISO group, whereas total Smad3 expression did not change in all groups. When TGF-β2 inhibitor, pirfenidone, or Smad3 inhibitor, SIS3 HCl, were administered, the expression levels of p-Smad3 and Gli1 were reduced, and surviving pyramidal neurons decreased. By contrast, the expression levels of TGF-β2 and p-Smad3 did not change significantly after pre-injection of Smo inhibitor cyclopamine, but reduced the expression levels of Shh, Ptch, and Gli1. Moreover, Gli showed the lowest expression levels with pirfenidone combined with cyclopamine. These findings indicate that the TGF-β and hedgehog signaling pathways mediate the neuroprotection of ISO post-conditioning after cerebral I/R injury, and crosstalk between two pathways at the Gli1 level.

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Isoflurano fornece neuroproteção em lesão cerebral hipóxico‐isquêmica neonatal por inibição da apoptose

Abstract: Isoflurane showed a neuro-protective effect on hippocampal neuron injury induced by hypoxia through suppression of apoptosis.

Cited by 14 publications

References 37 publications

Protective effect of isoflurane preconditioning on neurological function in rats with HIE

Protective effect of isoflurane preconditioning on neurological function in rats with HIE

Opioids Preconditioning Upon Renal Function and Ischemia-Reperfusion Injury: A Narrative Review

TGF-β2 Induces Gli1 in a Smad3-Dependent Manner Against Cerebral Ischemia/Reperfusion Injury After Isoflurane Post-conditioning in Rats

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