GLP-1RAs Ameliorates Lipotoxic Oxidative Stress by Regulating the LINC01180/miR-30b/CPT1A Pathway
10.11969/j.issn.1673-548X.2023.12.017
- VernacularTitle:GLP-1RAs通过调控LINC01180/miR-30b/CPT1A通路改善脂毒性氧化应激
- Author:
Zhiying ZHANG
1
;
Shuang YAN
Author Information
1. 150001 哈尔滨医科大学附属第四医院内分泌科
- Keywords:
GLP-1RAs;
LINC01180;
MiR-30b;
Carnitine palmitoyl transferase 1;
Lipotoxic oxidative stress
- From:
Journal of Medical Research
2023;52(12):76-82
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of glucagon-like peptide-1 receptor agonists(GLP-1 RAs)on lipotoxic oxida-tive stress in islet cells,and to explore whether the mechanism is related to the regulation of LINC01180/miR-30b/CPT1A pathway.Methods Gene chips and bioinformatics analysis predicted that LINC01180might regulate microRNA and related proteins.In vivo and in vitro modeling,the models were divided into control group,high-fat group and GLP-1 RAs group.The content of malondialdehyde(MDA)and the activity of total antioxidant capacity(T-AOC)were detected.Hematoxylin-eosin staining and immunohistochemical Reg3γ analysis were determined either.Real-time quantitative polymerase chain reaction(RT-qPCR)was used to detect the expres-sion levels of LINC01180,miR-30b and CPT1A.The protein expression levels of CPT1A was detected by Western blot.LINC01180 was inhibited and overexpressed by transient transfection,the expression levels of miR-30b and CPT1A after transfection were detected by RT-qPCR.Results Bioinformatics analysis showed that LINC01180/miR-30b/CPTIA formed ceRNA regulatory network.The lipo-toxic oxidative stress was significantly improved in GLP-1RAs model,and the expression levels of LINC01180 was decreased,while the expression levels of miR-30b and CPT1A were increased.Transfection of LINC01180significantly affected the expression levels of miR-30b and CPT1 A.Conclusion GLP-1RAs ameliorates lipotoxic oxidative stress by down-regulating the expression levels of LINC01180 and up-regulating the expression of miR-30b and CPT1A.
