Dexmedetomidine Alleviates Hypoxic-Ischemic Brain Damage in Neonatal Rats Through Reducing MicroRNA-134-5p-Mediated NLRX1 Downregulation

Guan, Xiaohong; Zhou, Wen; Li, Lin; Peng, Qingxiong

doi:10.1016/j.jstrokecerebrovasdis.2022.106411

Cited by 5 publications

(5 citation statements)

References 41 publications

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“…More importantly, DEX has been reported to prevent of postoperative delirium and cognitive dysfunction [33]. [35,36]. Another research found that DEX could enhance miR-429-3p level which may contribute to attenuate cognitive impairment caused by cisplatin [37].…”

Section: Discussionmentioning

confidence: 99%

“…For instance, Li et al reported that DEX could downregulate miR-27a-3p level to deplete inflammation and autophagy in traumatic brain injury [ 34 ]. Guan et al and He et al uncovered that miR-134a-5p and miR-20a-5p expressions were depleted by DEX, thereby alleviate hypoxia-ischemic brain injury [ 35 , 36 ]. Another research found that DEX could enhance miR-429-3p level which may contribute to attenuate cognitive impairment caused by cisplatin [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

“…For instance, Li et al [ 34 ] elucidated that enhanced miR-146a-5p by exosomes could inhibit neurogenesis, thereby alleviating depression process. Guan et al [ 35 ] illustrated that miR-146a-5p might be a feasible antidepressant factor. In this study, we discovered that DEX could increase miR-146a-5p level during ECT treatment, which were in concordance with previous studies [ 38 , 39 ].…”

Section: Discussionmentioning

confidence: 99%

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Dexmedetomidine Regulates the miR-146a-5p/NF-κB Axis to Alleviate Electroconvulsive Therapy-Induced Cognitive Impairments

Zhou

Wang

et al. 2022

Computational and Mathematical Methods in Medicine

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Electroconvulsive therapy (ECT) is a nonpharmacological treatment for depressive episodes and other psychiatric disorders. It is used to control the condition by causing a transient loss of consciousness through electrical stimulation. Dexmedetomidine (DEX) is a novel and highly selective adrenergic agonist with sedative, sympathetic nerve activity inhibiting and stress-responsive effects. This study focused on the effect of DEX on cerebral protection after ECT treatment. 68 depression patients were enrolled and divided into control group and DEX group. The occurrence of delirium after ECT treatment in depression cases was recorded. In vivo, we constructed chronic mild and unpredictable stress (CUMS) rats to mimic depression model. Meanwhile, ECT treatment and DEX injection were administrated in CUMS rats. Learning and memory in rats were measured by Morris water maze test, open field test (OFT), and forced swimming test (FST). Finally, the expression of miR-146a-5p and NF-κB was determined by RT-qPCR and western blot assay. The incidence of delirium after ECT treatment was prominently reduced in DEX group in relation to control group. In vivo, DEX injection had no effect on ECT treatment efficacy against depression conditions. After ECT treatment, the cognitive impairment was ameliorated in CUMS rats accomplished with decreased miR-146a-5p and increased NF-κB level. Finally, compared with ECT treatment, DEX injection could protect against depression-like behaviors by increasing miR-146a-5p level and inactivated NF-κB pathway. Overall, ECT-induced cognitive impairment in depression rats could be ameliorated by DEX injection via miR-146a-5p/NF-κB axis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Dexmedetomidine Regulates the miR-146a-5p/NF-κB Axis to Alleviate Electroconvulsive Therapy-Induced Cognitive Impairments

Zhou

Wang

et al. 2022

Computational and Mathematical Methods in Medicine

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“…Overexpression of miR-134 negatively affects and impairs neuronal formation in the postnatal mouse brain [49]. The study demonstrates that miR-134-5 expression is increased and mediates hypoxicischemic brain injury and neuronal death via the C/EBPα/miR-134-5p/KPNA3 axis in pheochromocytoma (PC12) cells [50] and inhibition of NLRX1 expression [51] in a neonatal rat model of HIE. However, overexpression of miR-134 did not affect astrocyte survival but decreased extracellular glutamate concentration and promoted astrocyte maturation by increasing GLT-1 [52].…”

Section: Mirnasmentioning

confidence: 81%

Role and Therapeutic Potential of Non-coding RNAs in Astrocytes during Neonatal Brain Injury

Ye,

Yuan

2023

Preprint

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Perinatal brain injury is a major public health problem burdened with high morbidity, mortality and severe neurological sequelae. Despite advances in neonatal life-saving technologies, neonatal encephalopathy lacks specific and effective treatment. Therefore, mechanisms of central nervous system changes associated with perinatal brain injury have been a hot topic of neonatology research. In recent years, researchers have shifted more focus from neurons themselves to perineuronal cells and intercellular interactions. As a member of the nervous system network, astrocytes are one of the dominant glial cells that regulate ion homeostasis, blood flow, and antioxidant function in the brain. Their changes in molecular mechanisms (e.g., alterations in RNA regulatory networks) during brain injury storms deserve further attention. Non-coding RNAs participate in and promote reactive pathophysiologic changes in astrocytes. The review summarizes and discusses the role of non-coding RNAs in astrocytes in recent years in studies of neonatal brain injury. It focuses on the most studied disease-related ncRNAs: miRNAs, lncRNAs and circRNAs, and hopes to provide possible directions for pathophysiological studies and therapeutic approaches of neonatal brain injury.

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“…Nucleotide-binding oligomerization domain-like receptor (NLR) X1 (NLRX1), a mitochondrial nucleotidebinding oligomerization domain-like receptor (NLR) has been implicated in various inflammatory conditions (7)(8)(9). In the central nervous system (CNS) of animals and humans, NLRX1 was shown to be expressed ubiquitously in the whole brain, cortical, and hippocampal tissues in addition to a variety of cells such as neurons, astrocytes, and microglia (10)(11)(12)(13). It has been reported that NLRX1 can activate or suppress toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/tumor necrosis factor receptor-associated factor 6 (TRAF6)/inhibitor of κB kinase (IKK)/nuclear factor-κB (NF-κB) pathway depending on experimental conditions (14)(15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

NLRX1 ligand, docosahexaenoic acid, ameliorates LPS-induced inflammatory hyperalgesia by decreasing TRAF6/IKK/IκB-α/NF-κB signaling pathway activity

Dilsah Ezgi Yilmaz,

Sefika Pinar Senol,

Meryem Temiz-Resitoglu

et al. 2023

Cell Mol Biol (Noisy-le-grand)

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Dexmedetomidine Alleviates Hypoxic-Ischemic Brain Damage in Neonatal Rats Through Reducing MicroRNA-134-5p-Mediated NLRX1 Downregulation

Cited by 5 publications

References 41 publications

Dexmedetomidine Regulates the miR-146a-5p/NF-κB Axis to Alleviate Electroconvulsive Therapy-Induced Cognitive Impairments

Dexmedetomidine Regulates the miR-146a-5p/NF-κB Axis to Alleviate Electroconvulsive Therapy-Induced Cognitive Impairments

Role and Therapeutic Potential of Non-coding RNAs in Astrocytes during Neonatal Brain Injury

NLRX1 ligand, docosahexaenoic acid, ameliorates LPS-induced inflammatory hyperalgesia by decreasing TRAF6/IKK/IκB-α/NF-κB signaling pathway activity

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