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자료유형
학술저널
저자정보
Guang Yang (Shanxi Medical University) Yuan Zhao (Shanxi Children’s Hospital)
저널정보
연세대학교 의과대학 Yonsei Medical Journal Yonsei Medical Journal 제61권 제8호
발행연도
2020.1
수록면
660 - 669 (10page)

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Purpose: Neonatal hypoxic ischemic encephalopathy (HIE) is an essential factor underlying neonatal death and disability. Thisstudy sought to explore the role of miR-146b-5p in regulating neonatal HIE. Materials and Methods: In vitro and in vivo HIE models were established in PC12 cells and 10-day neonatal Sprague Dawley rats,respectively. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to assess miR-146b-5p expressionand inflammatory factors [interleukin (IL)-6 and tumor necrosis factor (TNF)-α] in brain lesions and PC12 cells, while enzymelinkedimmunosorbent assay was employed to detect the expression of oxidative stress factors (SOD and GSH-Px). Gain- andloss-assays of miR-146b-5p were conducted to verify its role in modulating the viability and apoptosis of PC12 cells under oxygenglucosedeprivation (OGD) treatment. Expression of TLR4, IRAK1, TRAF6, TAK1, and NF-κB were examined by qRT-PCR and/orWestern blot. Dual luciferase activity assay was conducted to identify relationships between miR-146b-5p and IRAK1. Results: In the HIE models, significant oxidative stress and inflammatory responses emerged upon upregulation of TLR4/IRAK1/TRAF6/TAK1/NF-κB signaling. Overexpression of miR-146b-5p greatly inhibited OGD-induced PC12 cell injury, inflammatoryresponses, and oxidative stress. Inhibiting miR-146b-5p, however, had the opposite effects. IRAK1 was found to be a target of miR-146b-5p, and miR-146b-5p overexpression suppressed the activation of IRAK1/TRAF6/TAK1/NF-κB signaling. Conclusion: This study demonstrated that miR-146b-5p overexpression alleviates HIE-induced neuron injury by inhibiting theIRAK1/TRAF6/TAK1/NF-κB pathway.

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