文献类型：期刊文献

英文题名：Icariin attenuates diabetic cardiomyopathy by inhibiting NLRP3 inflammasome through SIRT3-mediated TFAM deacetylation

作者：Sun, Min[1,2];Huang, Hui[1];Wei, Chao[3];Xing, Yuan[4];Wu, Bing[1,2]

第一作者：孙梅;Sun, Min

通信作者：Wu, B[1];Wu, B[2];Xing, Y[3]

机构：[1]940th Hosp Joint Logist Support Force Chinese Peop, Dept Geriatr, Lanzhou, Peoples R China;[2]Gansu Univ Tradit Chinese Med, Clin Med Coll 1, Lanzhou, Peoples R China;[3]Chinese Peoples Liberat Army Gen Hosp, Med Ctr 2, Dept Neurol, Beijing, Peoples R China;[4]940th Hosp Joint Logist Support Force Chinese Peop, Dept Clin Lab, Key Lab Stem Cells & Gene Grug Gansu Prov, Lanzhou, Peoples R China

第一机构：940th Hosp Joint Logist Support Force Chinese Peop, Dept Geriatr, Lanzhou, Peoples R China

通信机构：[1]corresponding author), 940th Hosp Joint Logist Support Force Chinese Peop, Dept Geriatr, Lanzhou, Peoples R China;[2]corresponding author), Gansu Univ Tradit Chinese Med, Clin Med Coll 1, Lanzhou, Peoples R China;[3]corresponding author), 940th Hosp Joint Logist Support Force Chinese Peop, Dept Clin Lab, Key Lab Stem Cells & Gene Grug Gansu Prov, Lanzhou, Peoples R China.|[10735]甘肃中医药大学;

年份：2026

卷号：17

外文期刊名：FRONTIERS IN PHARMACOLOGY

收录：;Scopus(收录号：2-s2.0-105042386975);WOS:【SCI-EXPANDED(收录号:WOS:001791495000001)】；

基金：The author(s) declared that financial support was received for this work and/or its publication. This project was sponsored by Natural Science Foundation of Gansu Province (25JRRA425, 23JRRA1671), the Project of Northwest Minzu University (31920240058), the 940th Hospital of Joint Logistic Support Force highlevel personnel training program (Nos. 2024-G2-7) and Scientific Research Project on Health Industry of Gansu Province (GSWSKY2025-55).

语种：英文

外文关键词：diabetic cardiomyopathy; icariin; mitochondrial DNA; NLRP3; oxidative stress; sirt3; TFAM

摘要：Introduction Icariin (ICA), a major flavonoid isolated from the traditional oriental herbal medicine Epimedium, exhibits various pharmacological activities, including anti-inflammatory and antioxidant properties. It has been demonstrated in previous studies that the NLRP3 inflammasome contributes to the progression of diabetic cardiomyopathy (DCM), and that ICA exerts a protective effect in DCM. However, the mechanism by which ICA may attenuate DCM by inhibiting the NLRP3 inflammasome still needs to be elucidated.Methods The effects of ICA on the cardiac function and pathology of db/db mice were investigated. Levels of mitochondrial reactive oxygen species (mtROS), mitochondrial DNA (mtDNA), the NLRP3 inflammasome and pyroptosis were monitored in the hearts of DCM mice or H9c2 cardiomyoblasts induced by hyperglycaemia following ICA treatment. Furthermore, sirtuin 3 (SIRT3) activity and expression, as well as mitochondrial transcription factor A (TFAM) acetylation, were detected following ICA treatment.Results We found that db/db mice treated with ICA exhibited significantly reduced cardiac hypertrophy and fibrosis, as well as improved cardiac function. ICA was associated with reduced mtROS, cytosolic mtDNA, NLRP3 inflammasome activation, and pyroptosis in the hearts of DCM mice or hyperglycaemia-induced H9c2 cardiomyoblasts, which may occur in a SIRT3-dependent manner. Ultimately, ICA-induced SIRT3 activation was associated with the deacetylation of TFAM. Discussion: These results suggested that ICA may attenuate DCM by inhibiting the NLRP3 inflammasome through a potential SIRT3-associated TFAM deacetylation pathway.