Isoflurane provides neuroprotection in neonatal hypoxic ischemic brain injury by suppressing apoptosis

Zhao, Dean; Bi, Lingyun; Huang, Qian; Zhang, Fangmin; Zi-ming, Han

doi:10.1016/j.bjane.2015.04.008

Cited by 19 publications

(18 citation statements)

References 37 publications

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“…It is important to note that isoflurane was used during the HIE procedure, which potentially could have masking effects to some of the phenotypes shown in this report. Isoflurane has neuroprotective effects in neonatal hypoxic-Ischemic brain injury 55 . Another limitation of this study is that Fig.…”

Section: Discussionmentioning

confidence: 99%

Attenuation of Retinal Vascular Development in Neonatal Mice Subjected to Hypoxic-Ischemic Encephalopathy

Zaitoun

Çıkla

Zafer

et al. 2018

Sci Rep

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A significant proportion of children that survive hypoxic-ischemic encephalopathy (HIE) develop visual impairment. These visual deficits are generally attributed to injuries that occur in the primary visual cortex and other visual processing systems. Recent studies suggested that neuronal damage might also occur in the retina. An important structure affecting the viability of retinal neurons is the vasculature. However, the effects of HIE on the retinal neurovasculature have not been systemically evaluated. Here we investigated whether exposure of postnatal day 9 (P9) neonatal mice to HIE is sufficient to induce neurovascular damage in the retina. We demonstrate that the blood vessels on the surface of the retina, from mice subjected to HIE, were abnormally enlarged with signs of degeneration. The intermediate and deep vascular layers in these retinas failed to form normally, particularly in the periphery. All the vascular damages observed here were irreversible in nature up to 100 days post HIE. We also observed loss of retinal neurons, together with changes in both astrocytes and Müller cells mainly in the inner retina at the periphery. Collectively, our findings suggest that HIE results in profound alterations in the retinal vasculature, indicating the importance of developing therapeutic strategies to protect neurovascular dysfunction not only in the brain but also in the retina for infants exposed to HIE.

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Section: Discussionmentioning

confidence: 99%

Attenuation of Retinal Vascular Development in Neonatal Mice Subjected to Hypoxic-Ischemic Encephalopathy

Zaitoun

Çıkla

Zafer

et al. 2018

Sci Rep

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“…Third, recent studies have found that general anesthesia may have some advantages over conscious sedation. Some animal studies have found that inhaled anesthetics, such as isoflurane, have neuroprotective effects by inhibiting neuronal apoptosis [30]. In addition, some studies suggest that appropriate exposure to inhaled anesthetics can inhibit reductions in astroglial processes and reduce glial scarring, which can lead to long-term neurological recovery after stroke [31].…”

Section: Discussionmentioning

confidence: 99%

General Anesthesia may have Similar Outcomes with Conscious Sedation in Thrombectomy Patients with Acute Ischemic Stroke: A Real-World Registry in China

et al. 2018

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Background and Purpose: Clinical trials showed that anesthesia may not influence the functional outcome in stroke patients with endovascular therapy; however, data are lacking in China. Using real-world registry data, our study aims to compare the effects of general anesthesia or conscious sedation on functional outcomes in stroke patients treated with thrombectomy in China. Methods: Consecutive patients with acute anterior circulation stroke receiving thrombectomy in 21 stroke centers between January 2014 and June 2016 were included in this study. The propensity score analysis with 1: 1 ratio was used to match the baseline variables between patients with general anesthesia and the conscious sedation. The 90-day modified Rankin Scale (mRS), symptomatic intracranial hemorrhage (sICH), and death were compared between groups. Results: Of the 698 patients undergoing endovascular treatment, 138 were treated with general anesthesia and 560 with conscious sedation. After propensity score matching, 114 general anesthesia and 114 conscious sedation patients were matched. The proportions of patients with 90-day mRS 0–2 were not significantly different between general anesthesia and conscious sedation groups (41.2% [47/114] vs. 46.5% [53/114], p = 0.470), nor were the rates of sICH (21.9% [25/114] vs. 12.3% [14/114], p = 0.072) and 90-day mortality (31.6% [36/114] vs. 21.9% [25/114], p = 0.145). Conclusion: Anesthesia patterns may have no significant impacts on clinical outcomes in patients with acute anterior circulation occlusion stroke undergoing endovascular treatment in the real-world practice in China.

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“…The incision was sutured and the pups were placed in their respective cages and were allowed to recover for 2 h. The pups were then placed in a temperature-controlled chamber and subjected to 8% O 2 and 92% N 2 for 2 h at 37°C. At 3 h after insult, a separate group of pups were exposed to isoflurane (1.5% with air as carrier; gas flow 2 L/min) continuously for 6 h [1,34]. After 6 h of isoflurane exposure, the rats were removed from the chamber and exposed to air.…”

Section: Methodsmentioning

confidence: 99%

Mangiferin Potentiates Neuroprotection by Isoflurane in Neonatal Hypoxic Brain Injury by Reducing Oxidative Stress and Activation of Phosphatidylinositol-3-Kinase/Akt/Mammalian Target of Rapamycin (PI3K/Akt/mTOR) Signaling

Wang

Long

et al. 2018

Med Sci Monit

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BackgroundHypoxic-ischemic brain injury in the perinatal period is a main cause of perinatal mortality and neurologic complications in neonates and children. Recent studies have focused on the neuroprotective effect of anesthetic drugs. The volatile anesthetic isoflurane has been shown to exert neuroprotective effects in cerebral ischemia. Mangiferin is a natural polyphenol with various pharmacological properties, including antioxidant and ant-tumor effects. This study aimed to determine whether mangiferin potentiates the neuroprotective effects of isoflurane and also if mangiferin when administered alone exerts neuroprotective effects following hypoxic-ischemic brain injury.Material/MethodsSprague-Dawley rats were subjected to cerebral hypoxic ischemia on postnatal day 10 (P10). Mangiferin (50, 100, or 200 mg/kg b.w.) was intragastrically administered from P3 to P12 and 1 h prior to insult on the day of ischemic induction. At 3 h after hypoxia-ischemia (HI) insult, separate groups of rat pups were exposed to isoflurane (1.5%) for 6 h. Following 48 h of HI, the rats were sacrificed and brain tissues were used for analysis.ResultsMangiferin treatment attenuated neuronal apoptosis and reduced cerebral infarct volume. The expression of cleaved caspase-3 and apoptotic cascade proteins were regulated. The levels of reactive oxygen species (ROS) and malondialdehyde were reduced by mangiferin and/or isoflurane exposure. The levels of antioxidant glutathione were considerably raised under HI injury, which was modulated by mangiferin and isoflurane exposure. The PI3K/Akt signaling pathway, which was downregulated following HI insult, was activated by mangiferin and/or isoflurane.ConclusionsThis study reveals the potent neuroprotective efficacy of mangiferin against HI-induced brain injury via effectively modulating apoptotic pathways, ROS levels, and PI3K/Akt cascades while potentiating protective effects of isoflurane.

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Isoflurane provides neuroprotection in neonatal hypoxic ischemic brain injury by suppressing apoptosis

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

Cited by 19 publications

References 37 publications

Attenuation of Retinal Vascular Development in Neonatal Mice Subjected to Hypoxic-Ischemic Encephalopathy

Attenuation of Retinal Vascular Development in Neonatal Mice Subjected to Hypoxic-Ischemic Encephalopathy

General Anesthesia may have Similar Outcomes with Conscious Sedation in Thrombectomy Patients with Acute Ischemic Stroke: A Real-World Registry in China

Mangiferin Potentiates Neuroprotection by Isoflurane in Neonatal Hypoxic Brain Injury by Reducing Oxidative Stress and Activation of Phosphatidylinositol-3-Kinase/Akt/Mammalian Target of Rapamycin (PI3K/Akt/mTOR) Signaling

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