Protective effect and mechanism of chemokine C-C motif ligand 6 on glucose and oxygen deprivation induced injury of cardiomyocytes
10.3760/cma.j.issn.1671-0282.2019.06.013
- VernacularTitle:趋化因子C-C基序配体6对心肌细胞糖氧剥夺损伤的保护作用和机制研究
- Author:
Yue LIU
1
;
Xiaoyan ZHANG
;
Changwei REN
;
Wenjun ZHU
;
Jiang DAI
;
Yongqiang LAI
Author Information
1. 首都医科大学附属北京安贞医院心脏外科 100029
- Keywords:
Cardiomyocytes;
Chemokine;
Apoptosis
- From:
Chinese Journal of Emergency Medicine
2019;28(6):724-728
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the protective effect of chemokine C-C motif ligand 6 (CCL6) on glucose-oxygen deprivation induced injury in cardiomyocytes and its possible molecular mechanism.Methods Gene expression was analyzed in the public database Gene Expression Omnibus (GEO) database and gene expression of analyzed for myocardial tissue was analyzed gene expression in the sham group and the ischemia-reperfusion group (IR group).Rat H9C2 cardiomyocytes were cultured in vitro,and myocardial cell injury model was established by oxygen glucose deprivation (OGD).Cell viability was detected by MTT assay;apoptosis was determined by Annex V/PI double staining;the expression of related genes was detected by real-time PCR and Western blot.Results Compared with the sham group,transcriptome analysis and real-time PCR showed that the expression of CCL6 in the myocardial tissue of the IR group was significantly decreased (P＜0.01).Oxygen glucose deprivation induced a decrease in CCL6 expression levels in H9C2 cardiomyocytes in a time-dependent manner.In addition,oxygen glucose deprivation leads to decreased cell viability and increased apoptosis;while addition of CCL6 promotes cell viability and reduces apoptosis.The IncRNA microarray and real-time PCR showed that CCL6 treatment of cardiomyocytes resulted in a significant decrease in the expression of hicRNA IGF2-AS and further increased the phosphorylation of Akt and GSK-3β.Conclusion CCL6 can inhibit cardiomyocyte injury induced by glucose deprivation,and its molecular mechanism may be related to inhibition of IGF2-AS and enhancement of Akt/GSK-3β signaling pathway.
