Costunolide alleviates hyperglycaemia-induced diabetic cardiomyopathy via inhibiting inflammatory responses and oxidative stress

doi:10.1111/jcmm.17686

科研成果详情

题名	Costunolide alleviates hyperglycaemia-induced diabetic cardiomyopathy via inhibiting inflammatory responses and oxidative stress
作者	Jin, Bo1,2; Chen, Yi 2; Wang, Jiong2; Chen, Yue 2; Zhang, Mengpei 1; Huang, Jianxiong 1; Wang, Yi1,2
发表日期	2023-03
发表期刊	Journal of cellular and molecular medicine 影响因子和分区
语种	英语
原始文献类型	Journal Article
关键词	Costunolide NF-κB Nrf-2 diabetic cardiomyopathy inflammation oxidative stress
其他关键词	NF-KAPPA-B ; MOLECULAR-MECHANISMS ; INJURY ; MELLITUS ; PROTECTS ; HEART ; MICE ; ROS
摘要	Hyperglycaemia-induced myocardial injury promotes the induction of heart failure in diabetic patients. Impaired antioxidant capability and sustained chronic inflammation play a vital role in the progression of diabetic cardiomyopathy (DCM). Costunolide (Cos), a natural compound with anti-inflammatory and antioxidant properties, has exhibited therapeutic effects in various inflammatory diseases. However, the role of Cos in diabetes-induced myocardial injury remains poorly understood. In this study, we investigated the effect of Cos on DCM and explored the potential mechanisms. C57BL/6 mice were administered intraperitoneal streptozotocin for DCM induction. Cos-mediated anti-inflammatory and antioxidation activities were examined in heart tissues of diabetic mice and high glucose (HG)-stimulated cardiomyocytes. Cos markedly inhibited HG-induced fibrotic responses in diabetic mice and H9c2 cells, respectively. The cardioprotective effects of Cos could be correlated to the reduced expression of inflammatory cytokines and decreased oxidative stress. Further investigations demonstrated Cos reversed diabetes-induced nuclear factor-κB (NF-κB) activation and alleviated impaired antioxidant defence system, principally via activation of nuclear factor-erythroid 2 p45-related factor-2 (Nrf-2). Cos alleviated cardiac damage and improved cardiac function in diabetic mice by inhibiting NF-κB-mediated inflammatory responses and activating the Nrf-2-mediated antioxidant effects. Therefore, Cos could be a potential candidate for the treatment of DCM.
资助项目	National Natural Science Foundation of China [81970338, 82170373]
出版者	WILEY
ISSN	1582-1838
EISSN	1582-4934
卷号	27 期号:6 页码:831-845
DOI	10.1111/jcmm.17686
页数	15
WOS类目	Cell Biology ; Medicine, Research & Experimental
WOS研究方向	Cell Biology ; Research & Experimental Medicine
WOS记录号	WOS:000936440500001
收录类别	PUBMED ; SCIE ; SCOPUS
在线发表日期	2023-02
URL	查看原文
PubMed ID	36810875
SCOPUSEID	2-s2.0-85148616399
通讯作者地址	[Huang, Jianxiong]The Affiliated Xiangshan Hospital of Wenzhou Medical University,Zhejiang,Ningbo,325035,China ; [Wang, Yi]The Affiliated Xiangshan Hospital of Wenzhou Medical University,Ningbo,China
Scopus学科分类	Molecular Medicine;Cell Biology
TOP期刊	TOP期刊
引用统计
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/172802
专题	药学院（分析测试中心）_生物有机与药物化学研究中心其他_附属象山医院（象山县第一人民医院）其他_附属萧山医院（杭州市萧山区第一人民医院）
通讯作者	Huang, Jianxiong; Wang, Yi
作者单位	1.The Affiliated Xiangshan Hospital of Wenzhou Medical University,Ningbo,China; 2.Chemical Biology Research Center,School of Pharmaceutical Sciences,Wenzhou Medical University,Wenzhou,China
第一作者单位	附属萧山医院（杭州市萧山区第一人民医院）; 附属象山医院（象山县第一人民医院）; 药学院（分析测试中心）; 生物有机与药物化学研究中心
通讯作者单位	附属萧山医院（杭州市萧山区第一人民医院）; 附属象山医院（象山县第一人民医院）
第一作者的第一单位	附属萧山医院（杭州市萧山区第一人民医院）
推荐引用方式 GB/T 7714	Jin, Bo,Chen, Yi,Wang, Jiong,et al. Costunolide alleviates hyperglycaemia-induced diabetic cardiomyopathy via inhibiting inflammatory responses and oxidative stress[J]. Journal of cellular and molecular medicine,2023,27(6):831-845.
APA	Jin, Bo., Chen, Yi., Wang, Jiong., Chen, Yue., Zhang, Mengpei., ... & Wang, Yi. (2023). Costunolide alleviates hyperglycaemia-induced diabetic cardiomyopathy via inhibiting inflammatory responses and oxidative stress. Journal of cellular and molecular medicine, 27(6), 831-845.
MLA	Jin, Bo,et al."Costunolide alleviates hyperglycaemia-induced diabetic cardiomyopathy via inhibiting inflammatory responses and oxidative stress".Journal of cellular and molecular medicine 27.6(2023):831-845.