Protective effect of liraglutide on the myocardium of type 2 diabetic rats by inhibiting polyadenosine diphosphate-ribose polymerase-1

doi:10.4239/wjd.v14.i2.110

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World Journal of Diabetes

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World J Diabetes. Feb 15, 2023; 14(2): 110-119
Published online Feb 15, 2023. doi: 10.4239/wjd.v14.i2.110

Protective effect of liraglutide on the myocardium of type 2 diabetic rats by inhibiting polyadenosine diphosphate-ribose polymerase-1

Dong-Dong Xue, Xiang Zhang, De-Wei Li, Yan-Lan Yang, Jing-Jin Liu

Dong-Dong Xue, Xiang Zhang, Jing-Jin Liu, Department of Endocrinology, Shanxi Provincial People's Hospital, Taiyuan 030000, Shanxi Province, China

De-Wei Li, Department of Thyroid Surgery, Shanxi Provincial People's Hospital, Taiyuan 030000, Shanxi Province, China

Yan-Lan Yang, Department of Endocrine, Shanxi Provincial People's Hospital, Taiyuan 030012, Shanxi Province, China

Author contributions: Xue DD and Zhang X contributed to the methodology; Yang YL and Liu JJ contributed to the writing original draft preparation; Li DW, Liu JJ contributed to the revising.

Supported by Shanxi Provincial Natural Science Foundation, No. 201701D121159; Shanxi Provincial Health and Family Planning Commission, No. 2014016; and Health Commission of Shanxi Province, No. 2019020.

Institutional animal care and use committee statement: All animal experiments conformed to the internationally accepted principles for the care and use of laboratory animals, protocol No. SYXK (Jin) 2018-1203, Animal Ethics Committee of Shanxi Provincial People's Hospital.

Conflict-of-interest statement: The authors declare no conflicts of interest.

Data sharing statement: The data to support the findings in the study are available from the corresponding author upon reasonable request.

Corresponding author: Jing-Jin Liu, MD, Technician, Department of Endocrinology, Shanxi Provincial People's Hospital, No. 29 Shuangta Street, Taiyuan 030012, Shanxi Province, China. liumeng237237@163.com

Received: September 16, 2022
Peer-review started: September 16, 2022
First decision: November 18, 2022
Revised: November 26, 2022
Accepted: December 21, 2022
Article in press: December 21, 2022
Published online: February 15, 2023
Processing time: 151 Days and 9.9 Hours

ARTICLE HIGHLIGHTS

Research background

Glucagon-like peptide-1 (GLP-1) can reduce the apoptosis of islet microcirculation endothelial cells and protect islet tissue through the polyadenosine diphosphate-ribose polymerase-1 (PARP-1)/iNOs pathway.

Research motivation

Whether GLP-1 can protect cardiomyocytes by inhibiting the expression of PARP-1 is still unclear.

Research objectives

This study investigated the mechanism of liraglutide in improving myocardial injury in type 2 diabetic rats, further clarified the protective effect of liraglutide on the heart, and provided a new option for the treatment of diabetic cardiomyopathy (DCM).

Research methods

After successful modeling, the rats were fed a high-glucose and high-fat diet for 8 wk and then started drug intervention. Blood samples were collected from the abdominal aorta to detect fasting blood glucose and lipid profiles. Intact heart tissue was dissected, and its weight was used to calculate the heart weight index. Hematoxylin and eosin staining was used to observe the pathological changes in the myocardium and the expression of PARP-1 in the heart by immunohistochemistry.

Research results

After liraglutide intervention, compared with the model group, the expression of PARP-1 in myocardial tissue was decreased, and the reduction was more obvious in the high-dose group (P < 0.05) but still higher than that in the normal control group.

Research conclusions

Liraglutide may improve myocardial injury in type 2 diabetic rats by inhibiting the expression of myocardial PARP-1 in a dose-dependent manner.

Research perspectives

Through the detection of heart weight index, blood lipids, and PARP-1 expression and observation of cardiac pathological changes in this experiment, we found that liraglutide can delay the occurrence and development of DCM by reducing the expression of cardiac PARP-1, which provides evidence for its clinical application in DCM.