Downregulation of microRNA-448 improves isoflurane-induced learning and memory impairment in rats

Wu, Qun; Dai, Qinxue; Jiang, Lingzhi; Wang, Yichuan; Yang, Tao; Miao, Jianxia; Wang, Junlu; Yu, Han

doi:10.3892/mmr.2017.6724

Cited by 9 publications

(10 citation statements)

References 33 publications

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“…Notably, the involvement of miRNAs in anestheticinduced neuron injury has been proposed in recent researches. A study in isoflurane-treated rats reported that miR-448 knockdown suppressed neuron apoptosis, and further participated in the regulation of isofluraneinduced learning and memory impairment [13]. Another study about sevoflurane-induced cognitive dysfunction revealed that the addition of miR-96 promoted cell apoptosis induced by sevoflurane and exacerbated the cognitive function impairment of the rats [14].…”

Section: Discussionmentioning

confidence: 99%

“…In recent years, miRNAs have shown potential effect for the management of neurological diseases, including neuron injury induced by anesthesia [10][11][12]. For example, Wu et al have suggested that downregulation of miR-448 plays an important role in improving isoflurane-induced learning and memory impairment through regulating neuron apoptosis [13]. Another study in neonatal rats has also reported that the application of sevoflurane elevates the level of miR-96, which promotes hippocampal neuron apoptosis and weakens the learning and memory performance of the rats [14].…”

Section: Introductionmentioning

confidence: 99%

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Neuroprotective effects of miR-142-5p downregulation against isoflurane-induced neurological impairment

2020

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Background: Isoflurane can lead to neuron damage to the developing brain, resulting in learning and memory disability. The aim of this study was to investigate the role of miR-142-5p on isoflurane-induced neurological impairment. Methods: The Morris water maze (MWM) test was performed to evaluate spatial learning and memory of rats. The expression level of miR-142-5p was measured using qRT-PCR. MTT assay was used to calculate the viability of hippocampal neuronal cells. The cell apoptosis was analyzed using Flow cytometric assay. Results: Isoflurane treatment led to the increase of neurological function score and escape latency, and the reduction of time spent in the original quadrant in rats. The expression level of miR-142-5p was increased significantly in isoflurane-treated rats. MiR-142-5p downregulation protected against isoflurane-induced neurological impairment, which was reflected by the decrease of neurological function score and escape latency, and the increase of time spent in the original quadrant. In vitro, downregulation of miR-142-5p alleviated isoflurane-induced neuron cell viability inhibition, and relieved isoflurane-induced cell apoptosis. Conclusions: MiR-142-5p downregulation plays a neuroprotective role in protecting against isoflurane-induced neurological impairment through regulating neuron cell viability and apoptosis. It provides a theoretical basis for the investigation of the mechanism underlying the effect on isoflurane-induced neurological impairment.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Neuroprotective effects of miR-142-5p downregulation against isoflurane-induced neurological impairment

2020

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“…MiR-124 promoted cell proliferation and inhibited cell apoptosis of hippocampal neurons via regulation of early growth response 1, thus improving spatial learning and memory ability damaged by isoflurane (Yang et al, 2019). Decrease of miR-448 attenuated learning and memory impairment induced by isoflurane (Wu et al, 2017). However, whether miRNAs are associated with isoflurane-related cognitive dysregulation in diabetes has not been reported yet.…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, anesthetics have certain effects on the expression level of miRNAs in the brain (Lu et al, 2015). Further studies have shown the correlation between the expression of several miRNAs and isoflurane-related cognitive disorders, such as miRNA-153 (Shao et al, 2019), miR-124 (Yang et al, 2019) and miR-488 (Wu et al, 2017). MiR-153 protected against neurotoxicity induced by isoflurane via inhibition of neurocyte apoptosis and promotion of cell proliferation (Shao et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Isoflurane-induced expression of miR-140-5p aggravates neurotoxicity in diabetic rats by targeting SNX12

et al. 2020

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-MicroRNAs (miRNAs) are widely known as critical regulators in isoflurane-induced neurotoxicity during the development of brain. Moreover, isoflurane could aggravate cognitive impairment in diabetic rats. The present study was designed to investigate the role and mechanism of miR-140-5p on isoflurane-induced neurotoxicity in diabetic rats. Firstly, a diabetic rat model was established by injection of streptozotocin (STZ) and identified by Morris water maze test. The result indicated that isoflurane treatment exacerbated STZ-induced cognitive impairment, as demonstrated by increase of the latency to the platform and decrease of the proportion of time spent in the target quadrant. Secondly, miR-140-5p was up-regulated in diabetic rats treated with isoflurane. Functional assays revealed that knockdown of miR-140-5p attenuated neurotoxicity in diabetic rats, which was shown by a decrease of the latency to the platform and an increase of the proportion of time spent in the target quadrant. Mechanistically, we demonstrated that miR-140-5p directly bonded to SNX12 (sorting nexin 12). At last, the neuroprotective effect of miR-140-5p knockdown against isoflurane-aggravated neurotoxicity in diabetic rats was dependent on up-regulation of SNX12 and inhibition of cell apoptosis. In summary, these meaningful results demonstrated the mitigation of miR-140-5p knockdown against isoflurane-aggravated neurotoxicity in diabetic rats via SNX12, suggesting a novel target for neuroprotection in diabetes under isoflurane treatment.

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“…In this study, we induced isoflurane exposure (for 6 hr) models in neonatal SD rats aged 7 days. Recent studies have highlighted the regulatory roles of microRNAs (miRNAs) in neuron apoptosis and cognitive dysfunction triggered by anesthesia, including isoflurane (Li, Li, Zhuang, & Li, ; Wang, Ding, Lai, Liu, & Shuai, ; Wang, Zheng, Wu, & Niu, ; Wu et al, ).…”

Section: Introductionmentioning

confidence: 99%

microRNA‐124 attenuates isoflurane‐induced neurological deficits in neonatal rats via binding to EGR1

Yang

Guo

et al. 2019

Journal Cellular Physiology

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Isoflurane anesthesia induces neuroapoptosis in the development of the brain. In this study, neonatal rats and hippocampal neurons were subjected to isoflurane exposure, in which the effect of miR-124 on the neurological deficits induced by isoflurane was evaluated. Isoflurane anesthesia models were induced in neonatal SD rats aged 7 days and then treated with miR-124 agomir, miR-124 antagomir, or LV-CMV-early growth response 1 (EGR1) plasmids. Then, the spatial learning and memory ability of rats were evaluated by Morris water maze. Furthermore, primary hippocampal neurons cultured 7 days were also exposed to isoflurane and transfected with miR-124 agomir, miR-124 antagomir, or LV-CMV-EGR1 plasmids. The targeting relationship of miR-124 and EGR1 was verified by the dual-luciferase reporter gene assay. To identify the effect of miR-124 on neuron activities, the viability and apoptosis of hippocampal neurons were assessed. In response to isoflurane exposure, miR-124 expression was reduced and EGR1 expression was increased in the hippocampal tissues and neurons. The isoflurane anesthesia damaged rats' spatial learning and memory ability, and reduced viability, and promoted apoptosis of hippocampal neurons. EGR1 was targeted and negatively regulated by miR-124. The treatment of miR-124 agomir improved rats' spatial learning and memory ability and notably increased hippocampal neuron viability and resistance to apoptosis, corresponding to an increased brain-derived neurotrophic factor (BDNF) expression, inhibited expression of proapoptotic factors (cleaved-Caspase-3 and Bax), and enhanced the expression of antiapoptotic factor (Bcl-2). Upregulated miR-124 inhibited the expression of EGR1, by which mechanism miR-124 reduced the neurological deficits induced by isoflurane in neonatal rats through inhibiting apoptosis of hippocampal neurons.

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Downregulation of microRNA-448 improves isoflurane-induced learning and memory impairment in rats

Cited by 9 publications

References 33 publications

Neuroprotective effects of miR-142-5p downregulation against isoflurane-induced neurological impairment

Neuroprotective effects of miR-142-5p downregulation against isoflurane-induced neurological impairment

Isoflurane-induced expression of miR-140-5p aggravates neurotoxicity in diabetic rats by targeting SNX12

microRNA‐124 attenuates isoflurane‐induced neurological deficits in neonatal rats via binding to EGR1

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