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Neuroprotective effect of miR-410-3p against sevoflurane anesthesia-induced cognitive dysfunction in rats through PI3K/Akt signaling pathway via targeting C?X?C motif chemokine receptor 5

Genes & Genomics 2019년 41권 10호 p.1223 ~ 1231
 ( Su Rui ) - Huazhong University of Science and Technology Tongji Medical College Wuhan Children’s Hospital Department of Anesthesiology

 ( Sun Ping ) - Wuhan University Wuhan Third Hospital-Tongren Hospital Department of Anesthesiology
 ( Zhang Dianhong ) - Hospital of Shunyi District Beijing Department of Anesthesiology
 ( Xiao Wei ) - Huazhong University of Science and Technology Tongji Medical College Central Hospital of Wuhan Department of Anaesthesiology
 ( Feng Chun ) - Huazhong University of Science and Technology Tongji Medical College Wuhan Children’s Hospital Department of Anesthesiology
 ( Zhong Liang ) - Huazhong University of Science and Technology Tongji Medical College Wuhan Children’s Hospital Department of Anesthesiology

Abstract


Background: Postoperative cognitive dysfunction (POCD) is a neurodegenerative disorder with impairment of cognition. Sevoflurane anesthesia has been found to lead to CD and microRNAs (miRNAs) were reported to affect cognitive function. This study investigates the neuroprotective effect against sevoflurane anesthesia-induced CD.

Methods: HE staining was used to detect the pathological change of hippocampal neuron. Morris water maze test was used to analyze latency time, platform crossing and swimming speed. Quantitative real-time PCR (qRT-PCR) and western blotting were performed to examine the mRNA and protein expression of miR-410-3p, IL-6, TNF-α, IL-1β and C?X?C motif chemokine receptor 5 (CXCR5). Dual-luciferase reporter assay was used to detect the relationship between miR-410-3p and CXCR5.

Results: MiR-410-3p was downregulated in sevoflurane anesthesia-induced rats and cells and act as a suppressor in sevoflurane anesthesia-induced hippocampal neuron apoptosis and inflammation. Furthermore, miR-410-3p was identified to bind with CXCR5. Further analysis showed that CXCR5 expression was increased by sevoflurane treatment, whereas was repressed by miR-410-3p overexpression. Moreover, miR-410-3p could inhibit sevoflurane anesthesia-induced hippocampal neuron apoptosis by phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway.

Conclusion: These data indicated that miR-410-3p exhibited its neuroprotective effect on sevoflurane anesthesia-induced CD by targeting CXCR5 via PI3K/Akt signaling pathway. Our study may potentially provide a new light on the pathogenesis and therapeutic method for sevoflurane anesthesia-induced CD.

키워드

Cognitive dysfunction; Sevoflurane; miR-410-3p; CXCR5; PI3K/Akt signaling pathway
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