Isoflurane postconditioning induces concentration- and timing-dependent neuroprotection partly mediated by the GluR2 AMPA receptor in neonatal rats after brain hypoxia–ischemia

Xu, Ying; Xue, Hang; Zhao, Ping; Yang, Yating; Ji, Guoyu; Yu, Weiwei; Han, Guang; Ding, Meng; Wang, Feifei

doi:10.1007/s00540-015-2132-7

Cited by 14 publications

(16 citation statements)

References 29 publications

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“…However, the improvement was limited (compared with sham group) but significant (compared with HI group) (Xu et al . ).…”

Section: Discussionmentioning

confidence: 97%

“…Equivalent amount of protein samples were separated by 10% sodium dodecyl sulfate‐polyacrylamide gels and then transferred onto polyvinylidene fluoride membranes (Xu et al . ). After blocking with 5% non‐fat milk, the membrane was incubated with the primary antibody overnight at 4°C.…”

Section: Methodsmentioning

confidence: 97%

“…The test was over when the rat fell down, or when the suspending time was more than 60 s, or when their posterior limbs caught the level (Xu et al . ).…”

Section: Methodsmentioning

confidence: 97%

“…The swimming routes and navigation positioning strategy were analyzed with image analysis software (Shanghai Mobiledatum Ltd, Shanghai City, China) (Xu et al . ).…”

Section: Methodsmentioning

confidence: 97%

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Autophagy activation involved in hypoxic‐ischemic brain injury induces cognitive and memory impairment in neonatal rats

Tian

et al. 2016

Journal of Neurochemistry

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Hypoxic-ischemic brain injury (HIBI) in neonates can lead to lifelong cognitive and memory impairment, but protective strategies are lacking at present. It has been demonstrated that autophagy plays a critical role in HIBI, while the function of autophagy in cognitive and memory impairment induced by HIBI in neonates has not been tested. In this study, we tested the impact of autophagy on the impairment of cognitive function and memory in HIBI neonatal rats by using a Morris water maze and investigated its possible mechanisms, which were established as HIBI model by ligating the left common carotid artery in neonatal rats, followed by 2-h hypoxia. The expression of microtubule-associated protein 1 light chain 3 (LC3)-II increased in HI group 24 h after HI in neonatal rats, while Sequestosome 1 (P62/SQSTM1), phosphorylated cAMP-response element-binding protein (p-CREB) decreased (compared with the sham group, p < 0.05), which were shown in the same left hippocampus CA3 region by immunofluorescence analysis. Brain injury of neonatal rats was aggravated significantly at 7 day after HI, coinciding with the results of Morris water maze. An autophagy inhibitor, 3-methyladenine (3-MA) pretreatment significantly attenuated the increase of LC3II and the loss of P62/SQSTM1 and p-CREB, ameliorated neuronal death, and improved the results of Morris water maze. Our results demonstrate that HIBI in neonatal rats induced excessive autophagy flux, which aggravated brain injury and induced cognitive and memory impairment during adolescence. Inhibition of autophagy reversed the results partly and improved the function of spatial learning and memory by attenuating the reduction of p-CREB. The use of autophagy modulators in the immature brain would create new opportunities for protective strategies clinically in the future.

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“…However, the improvement was limited (compared with sham group) but significant (compared with HI group) (Xu et al . ).…”

Section: Discussionmentioning

confidence: 97%

Section: Methodsmentioning

confidence: 97%

“…The test was over when the rat fell down, or when the suspending time was more than 60 s, or when their posterior limbs caught the level (Xu et al . ).…”

Section: Methodsmentioning

confidence: 97%

“…The swimming routes and navigation positioning strategy were analyzed with image analysis software (Shanghai Mobiledatum Ltd, Shanghai City, China) (Xu et al . ).…”

Section: Methodsmentioning

confidence: 97%

See 2 more Smart Citations

Autophagy activation involved in hypoxic‐ischemic brain injury induces cognitive and memory impairment in neonatal rats

Tian

et al. 2016

Journal of Neurochemistry

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“…This finding suggests that higher concentration of isoflurane may not provide better neuroprotection 3233. (5) Xu et al34 investigated the concentrations and time windows of isoflurane post-conditioning in neonatal cerebral HI. In their experiment, 7-day-old rats were randomly divided into eight groups ( n = 40 per group).…”

Section: Experimental Studies In Isoflurane Post-conditioningmentioning

confidence: 99%

Neuroprotection provided by isoflurane pre-conditioning and post-conditioning

et al. 2017

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Isoflurane, a volatile and inhalational anesthetic, has been extensively used in perioperative period for several decades. A large amount of experimental studies have indicated that isoflurane exhibits neuroprotective properties when it is administrated before or after (pre-conditioning and post-conditioning) neurodegenerative diseases (e.g., hypoxic ischemia, stroke and trauma). Multiple mechanisms are involved in isoflurane induced neuroprotection, including activation of glycine and γ-aminobutyric acid receptors, antagonism of ionic channels and alteration of the function and activity of other cellular proteins. Although neuroprotection provided by isoflurane is observed in many animal studies, convincing evidence is lacking in human trials. Therefore, there is still a long way to go before translating its neuroprotective properties into clinical practice.

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Sustained Release of Dexamethasone from Sulfobutyl Ether β‐cyclodextrin Modified Self‐Assembling Peptide Nanoscaffolds in a Perinatal Rat Model of Hypoxia–Ischemia

Lü

Armstrong

Yager

et al. 2019

Adv Healthcare Materials

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Inflammation plays a critical role in the development of hypoxia–ischemia (HI) induced newborn brain damage. A localized, sustained delivery of dexamethasone (Dex) through an intracerebral injection could reduce the inflammatory response in the injured perinatal brain while avoiding unnecessary side effects. Herein, investigated using anionic sulfobutyl ether β‐cyclodextrin (SBE‐β‐CD) to load Dex in the (RADA)4 nanofiber networks as a means of reducing the inflammatory response to HI injury is investigated. The ionic interaction between SBE‐β‐CD and (RADA)4 dramatically affects nanofiber formation and the stability of the nanoscaffold is highly dependent on the SBE‐β‐CD/(RADA)4 ratio. It is observed that the Dex release rate is affected by the concentration of SBE‐β‐CD and (RADA)4 peptide. A higher concentration of SBE‐β‐CD or (RADA)4 results in a higher drug encapsulation efficiency and slower release rate of Dex. This phenomenon may be related to the structure of fiber bundles. Animal studies show that nanoscaffold loaded with Dex inhibits both microglia activation and glial scar formation compared to controls (Dex alone or nanoscaffold alone) within 2 days of injury. It is thought that this is a step toward building a multifaceted nanoscaffold that can be used to treat HI events in perinates.

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Isoflurane postconditioning induces concentration- and timing-dependent neuroprotection partly mediated by the GluR2 AMPA receptor in neonatal rats after brain hypoxia–ischemia

Abstract: Postconditioning with 1.5 and 2 % isoflurane affords neuroprotection in neonatal rats. The time window for isoflurane postconditioning to be effective against neonatal HI-induced brain injury was 0-6 h after HI. This protection may be mediated by GluR2-containing AMPARs.

Cited by 14 publications

References 29 publications

Autophagy activation involved in hypoxic‐ischemic brain injury induces cognitive and memory impairment in neonatal rats

Autophagy activation involved in hypoxic‐ischemic brain injury induces cognitive and memory impairment in neonatal rats

Neuroprotection provided by isoflurane pre-conditioning and post-conditioning

Sustained Release of Dexamethasone from Sulfobutyl Ether β‐cyclodextrin Modified Self‐Assembling Peptide Nanoscaffolds in a Perinatal Rat Model of Hypoxia–Ischemia

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