Wang Y.a· Zhao S.b· Li G.c· Wang D.d· Jin Y.b

Author affiliations

aDepartment of Operating Room, The Second Hospital of Shandong University, Shandong University, Jinan, China
bDepartment of Anesthesiology, The Second Hospital of Shandong University, Shandong University, Jinan, China
cDepartment of Anesthesiology, The Second Affiliated Hospital of Shandong First Medical University, Taian, China
dDepartment of Obstetrics, The Affiliated Hospital of Qingdao University, Qingdao, China

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Article / Publication Details

First-Page Preview

Received: July 28, 2021
Accepted: November 08, 2021
Published online: January 13, 2022

Number of Print Pages: 11
Number of Figures: 7
Number of Tables: 0

ISSN: 1021-7401 (Print)
eISSN: 1423-0216 (Online)

For additional information: https://www.karger.com/NIM

Abstract

Introduction: This article purposed to detect the function of the HOTAIR and HOTAIR/microRNA-129-5p (miR-129-5p) axis on the isoflurane (ISO)-injured cells and rat, and propounded a novel perspective in exploring the molecular pathogenesis of ISO damage. Methods: The expression of HOTAIR and miR-129-5p was tested by quantitative real-time PCR. The viable cells were identified using MMT, and the apoptotic cells were provided by flow cytometry. The concentration of proinflammatory indicators was revealed by enzyme-linked immunosorbent assay kits. The function of HOTAIR on oxidative stress was detected by commercial kits. A luciferase assay was performed to confirm the relationship between miR-129-5p and HOTAIR. The Morris water maze test was conducted to elucidate the cognition of SD rats. Results: The expression of HOTAIR was enhanced and the expression of miR-129-5p was lessened in the ISO-evoked SD rats and HT22 cells. The interference of HOTAIR reversed the injury of ISO on cell viability, apoptosis, inflammation, and oxidative stress. Besides, HOTAIR might be a target ceRNA of miR-129-5p. MiR-129-5p abrogated the function of silenced HOTAIR on cell viability, cell apoptosis, inflammation, and oxidative stress. Moreover, in vivo, the intervention of HOTAIR reversed the influence of ISO on cognition and oxidative stress by binding miR-129-5p. Discussion/Conclusion: Lowly expressed HOTAIR contributed to the recovery of the ISO-injured HT22 cell model from the abnormal viability, apoptosis, inflammation, and oxidative stress by regulating miR-129-5p. miR-129-5p mediated the function of HOTAIR on cognition and oxidative balance in the ISO-managed SD rat model.

© 2022 S. Karger AG, Basel

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First-Page Preview

Received: July 28, 2021
Accepted: November 08, 2021
Published online: January 13, 2022

Number of Print Pages: 11
Number of Figures: 7
Number of Tables: 0

ISSN: 1021-7401 (Print)
eISSN: 1423-0216 (Online)

For additional information: https://www.karger.com/NIM

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