Dexmedetomidine protects hepatic cells against oxygen-glucose deprivation/reperfusion injury via lncRNA CCAT1.

Abstract:

:Dexmedetomidine (Dex) protects different cell types during hypoxia or ischemia-reperfusion injury by inhibiting cell apoptosis. However, the underlying mechanism and its impact on hepatic ischemia reperfusion injury are still not known. In this study, we established a model of oxygen-glucose deprivation/reperfusion (OGD/R) injury in hepatocyte HL7702 cells, and studied the impact of Dex on cell proliferation, apoptosis, and cell cycle during OGD/R. In addition, we explored the role of CCAT1 in this process. We found that Dex increased cell proliferation and inhibited cell apoptosis during OGD/R, in a concentration-dependent manner. Dex partially reversed the OGD-inhibited expression of lncRNA CCAT1. Knockdown of CCAT1 by siRNA inhibited Dex-mediated protection against OGD/R-induced injury and promoted cell apoptosis, caspase-3 expression and cell cycle arrest in the G0/G1 phase, and inhibited cell proliferation and cyclin D1 expression. In contrast, overexpression of CCAT1 by pcDNA3.0-CCAT1 enhanced Dex-mediated protection against OGD/R-induced cell injury. Thus, Dex protects hepatocytes against OGD/R injury by upregulating lncRNA CCAT1. This study suggests a novel role of CCAT1 in ischemia reperfusion injury, and lays the framework for future studies.

journal_name

Cell Biol Int

authors

Zhou Z,Chen Q,Wan L,Zheng D,Li Z,Wu Z

doi

10.1002/cbin.10996

subject

Has Abstract

pub_date

2018-09-01 00:00:00

pages

1250-1258

issue

9

eissn

1065-6995

issn

1095-8355

journal_volume

42

pub_type

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