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BioMed Research International
Volume 2019, Article ID 1613820, 8 pages
https://doi.org/10.1155/2019/1613820
Research Article

Leukemia Inhibitory Factor Receptor Is Involved in Apoptosis in Rat Astrocytes Exposed to Oxygen-Glucose Deprivation

Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, China

Correspondence should be addressed to Hua Wang; gro.latipsoh-js@1hgnaw

Received 12 January 2019; Accepted 12 February 2019; Published 27 February 2019

Guest Editor: Hengjia Ni

Copyright © 2019 Liang Huo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Leukemia inhibitory factor (LIF) and leukemia inhibitory factor receptor (Lifr) protect CNS cells, specifically neurons and myelin-sheath oligodendrocytes, in conditions of oxygen-glucose deprivation (OGD). In the case of astrocyte apoptosis resulting from reperfusion injury following hypoxia, the function of the Lifr remains to be fully elucidated. This study established models of in vivo ischemia/reperfusion (I/R) using an in vitro model of OGD to investigate the direct impact of silencing the Lifr on astrocyte apoptosis. Astrocytes harvested from newborn Wistar rats were exposed to OGD. Cell viability and apoptosis levels were determined by the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and annexin V/propidium iodide (PI) staining assays, respectively. Apoptosis was further investigated by the TdT-mediated dUTP nick-end labelling (TUNEL) assay. A standard western blotting protocol was applied to determine levels of the protein markers Bcl2, Bax, p-Akt/Akt, p-Stat3/Stat3, and p-Erk/Erk. The cell viability assay (MTT) showed that astrocyte viability decreased in response to OGD. Furthermore, blocking RNA to silence the Lifr further reduces astrocyte viability and increases levels of apoptosis as detected by annexin V/PI double staining. Likewise, western blotting after Lifr silencing demonstrated increased levels of the apoptosis-related proteins Bax and p-Erk/Erk and correspondingly lower levels of Bcl2, p-Akt/Akt, and p-Stat/Stat3. The data gathered in these analyses indicate that the Lifr plays a pivotal role in the astrocyte apoptosis induced by hypoxic/low-glucose environments. Further investigation of the relationship between apoptosis and the Lifr may provide a potential therapeutic target for the treatment of neurological injuries.