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齐墩果酸在2型糖尿病患者中的心脏保护作用。

Cardioprotective role of oleanolic acid in patients with type 2 diabetes mellitus.

作者信息

Li Chengrui, He Jing, Li Yongjun, Zhang Chengyang, Wang Ziheng, Wu Xiaoman, Qi Fuwei

机构信息

Department of Anesthesiology, Lianshui People's Hospital Affiliated to Kangda College of Nanjing Medical University, Huai'an, China.

Department of Anesthesiology, The First People's Hospital of Taicang City, Taicang Affiliated Hospital of Soochow University, Suzhou, China.

出版信息

Heliyon. 2024 May 15;10(11):e31303. doi: 10.1016/j.heliyon.2024.e31303. eCollection 2024 Jun 15.

DOI:10.1016/j.heliyon.2024.e31303
PMID:38845938
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11153093/
Abstract

BACKGROUND

Patients with type 2 diabetes mellitus (T2DM) experience a decline in cardiac function, resulting in poor prognosis. Therefore, restoration of cardiac function and improvement of myocardial fibrosis is an important treatment goal for patients with T2DM.

MATERIAL AND METHODS

The chemical structure of oleanolic acid(OA) was downloaded from PubChem and uploaded to PharmMapper. GeneCards and OMIM databases were searched for genes related to OA and disease and plotted into a Venn diagram. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed using R software. Then, a mouse model of diabetes mellitus was established, and ELISA, echocardiographic analysis of cardiac function, TUNEL assay, and reactive oxygen species assay were performed.

RESULTS

Network pharmacology analysis identified the related targets and potential molecular mechanisms underlying the effects of OA in T2DM. ELISA, echocardiographic analysis of cardiac function, and TUNEL assay results showed that OA inhibits apoptosis and improves apoptotic indexes in mice with T2DM-induced myocardial injury.

CONCLUSION

The results demonstrate the myocardial protective effect of OA in this mouse model.

摘要

背景

2型糖尿病(T2DM)患者心脏功能会下降,导致预后不良。因此,恢复心脏功能和改善心肌纤维化是T2DM患者的重要治疗目标。

材料与方法

从PubChem下载齐墩果酸(OA)的化学结构并上传至PharmMapper。在GeneCards和OMIM数据库中搜索与OA和疾病相关的基因,并绘制维恩图。使用R软件进行基因本体(GO)和京都基因与基因组百科全书(KEGG)富集分析。然后,建立糖尿病小鼠模型,并进行酶联免疫吸附测定(ELISA)、心脏功能的超声心动图分析、末端脱氧核苷酸转移酶介导的缺口末端标记法(TUNEL)测定和活性氧测定。

结果

网络药理学分析确定了OA在T2DM中的相关靶点和潜在分子机制。ELISA、心脏功能的超声心动图分析和TUNEL测定结果表明,OA可抑制T2DM诱导的心肌损伤小鼠的细胞凋亡并改善凋亡指标。

结论

结果证明了OA在该小鼠模型中的心肌保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19cc/11153093/13970a93d68a/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19cc/11153093/f11a7dfcc4d4/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19cc/11153093/aaac93beda09/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19cc/11153093/c3b198096b0f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19cc/11153093/13970a93d68a/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19cc/11153093/f11a7dfcc4d4/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19cc/11153093/aaac93beda09/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19cc/11153093/c3b198096b0f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19cc/11153093/13970a93d68a/gr4.jpg

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