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    已发表论文

    IL-35 改善 2 型糖尿病诱导的心肌损伤小鼠的心肌应变:基于分层特异性应变的评估

     

    Authors Wang Z, Han L, Dong M, Liu Y, Hu X, Huang L, Zhang C, Guo L, Liu S, Liao L

    Received 17 December 2024

    Accepted for publication 29 April 2025

    Published 10 May 2025 Volume 2025:18 Pages 1551—1562

    DOI http://doi.org/10.2147/DMSO.S510594

    Checked for plagiarism Yes

    Review by Single anonymous peer review

    Peer reviewer comments 2

    Editor who approved publication: Dr Rebecca Conway

    Ziying Wang,1,* Leilei Han,2,* Mingyi Dong,3 Yunman Liu,2 Xiangsui Hu,1 Long Huang,4 Chunquan Zhang,1 Liangyun Guo,1 Shengbo Liu,5 Lingmin Liao1 

    1Department of Ultrasound, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of China; 2Department of Cardiology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of China; 3Department of Gastroenterology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of China; 4Department of Oncology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of China; 5GE Healthcare Ultrasound Application Specialist, Nanchang, People’s Republic of China

    *These authors contributed equally to this work

    Correspondence: Lingmin Liao, Department of Ultrasound, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 1, Minde Road, Donghu District, Nanchang, Jiangxi Province, People’s Republic of China, Tel +86-0791-13517097273, Email liaolingmin85@163.com

    Purpose: The established association between endothelial dysfunction and the pathogenesis of cardiovascular disease in diabetic individuals has been well-documented. Interleukin-35 (IL-35) can suppress inflammatory processes and ameliorate endothelial dysfunction. This study aimed to evaluate the effect of IL-35 treatment on diabetic mice with diabetes-induced cardiac injury using layer-specific strain analysis.
    Patients and Methods: Twenty-six mice were allocated into three groups: the control group (CON, n=10), the diabetic group (DM, n=10), and the diabetic group treated with IL-35 (DMIL, n=6). The DM and DMIL groups were subjected to a high-fat diet and streptozotocin to induce diabetes, with the DMIL group receiving an additional 6 weeks of IL-35 treatment. Measurements of body weight, blood glucose levels, routine echocardiographic parameters, and layer-specific strain were conducted at baseline, post-diabetes induction, and post-treatment. Morphological changes in cardiomyocytes were examined in pathological heart sections, and cardiac inflammation was detected by protein immunoblotting.
    Results: After inducing diabetes, diabetic mice exhibited notable systolic and diastolic dysfunction. IL-35 treatment significantly reduced myocardial inflammatory infiltration and improved myocardial fibrosis in the DMIL group in comparison to the DM group. Only diastolic function E/e’ showed a significant improvement when comparing conventional echocardiograms between the DMIL and DM groups. In the context of layered strain analysis, the DMIL group exhibited a notable enhancement in middle and epicardial global longitudinal strain and global radial strain when compared to the DM group.
    Conclusion: IL-35 can enhance myocardial function in diabetic mice. Layer-specific strain could serve as a valuable tool for evaluating interventions in diabetes.

    Keywords: diabetes mellitus, type 2, interleukin-35, global longitudinal strain, ventricular function, left

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