Epigallocatechin-3-gallate exerts cardioprotective effects related to energy metabolism in pressure overload-induced cardiac dysfunction

作者全名："Mou, Qiuhong; Jia, Zhongli; Luo, Min; Liu, Lingjuan; Huang, Xupei; Quan, Junjun; Tian, Jie"

作者地址："[Mou, Qiuhong; Jia, Zhongli; Luo, Min; Liu, Lingjuan; Tian, Jie] Chongqing Med Univ, Dept Cardiol, Childrens Hosp, Chongqing, Peoples R China; [Quan, Junjun] Chongqing Med Univ, Dept Anesthesiol, Childrens Hosp, Chongqing, Peoples R China; [Mou, Qiuhong; Luo, Min; Liu, Lingjuan; Quan, Junjun; Tian, Jie] Minist Educ, Key Lab Child Dev & Disorders, Chongqing, Peoples R China; [Mou, Qiuhong; Luo, Min; Liu, Lingjuan; Quan, Junjun; Tian, Jie] Natl Clin Res Ctr Child Hlth & Disorders, Chongqing, Peoples R China; [Mou, Qiuhong; Luo, Min; Liu, Lingjuan; Quan, Junjun; Tian, Jie] China Int Sci & Technol Cooperat Base Child Dev &, Chongqing, Peoples R China; [Mou, Qiuhong; Luo, Min; Liu, Lingjuan; Quan, Junjun; Tian, Jie] Chongqing Key Lab Pediat, Chongqing, Peoples R China; [Huang, Xupei] Florida Atlantic Univ, Charlie E Schmidt Coll Med, Boca Raton, FL USA; [Jia, Zhongli] Peoples Hosp Leshan, Dept Pediat, Sichuan, Peoples R China; [Tian, Jie] Chongqing Med Univ, Dept Cardiol, Childrens Hosp, 136 Zhongshan Er Rd, Chongqing 400014, Peoples R China; [Quan, Junjun] Chongqing Med Univ, Dept Anesthesiol, Childrens Hosp, 136 Zhongshan Er Rd, Chongqing 400014, Peoples R China"

通信作者："Tian, J (通讯作者)，Chongqing Med Univ, Dept Cardiol, Childrens Hosp, 136 Zhongshan Er Rd, Chongqing 400014, Peoples R China.; Quan, JJ (通讯作者)，Chongqing Med Univ, Dept Anesthesiol, Childrens Hosp, 136 Zhongshan Er Rd, Chongqing 400014, Peoples R China."

来源：ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS

ESI学科分类：BIOLOGY & BIOCHEMISTRY

WOS号：WOS:000802190200003

JCR分区：Q1

影响因子：3.9

年份：2022

卷号：723

期号：　

开始页：　

结束页：　

文献类型：Article

关键词：Pressure overload-induced cardiac dysfunction; Epigallocatechin-3-gallate; Cardiac remodeling; Energy metabolism; Ndufs4

摘要："Background: To investigate the mechanisms of potential cardioprotective effects of epigallocatechin-3-gallate (EGCG) in pressure overload-induced cardiac dysfunction. Methods: A chronic heart failure model was established using abdominal aortic constriction (AAC) surgery, rats were divided into sham, AAC, and AAC + EGCG groups. Echocardiography and tissue section staining were performed to evaluate cardiac function and pathology, respectively. Gene expression level were detected with quantitative real-time polymerase chain reactions. Label-free quantitative proteomics was used to investigate the whole proteomes of heart, and the differentially expressed proteins were analyzed using bioinformatics methods. Western blot was performed to validate the levels and the reliability of the differential proteins. Results: Compared with the AAC group, systolic dysfunction was improved in AAC + EGCG group after EGCG treatment. EGCG inhibited myocardial fibrosis and cardiac hypertrophy after AAC, along with reducing atrial natriuretic protein, B-type natriuretic peptide, collagen types 1 and 3 alpha 1, and transforming growth factor beta-1. Quantitative proteomics identified a total of 162 differentially expressed proteins, among them, 18 were closely related to cardiovascular disorders. Bioinformatics analyses showed that EGCG played a therapeutic role mainly by changing energy metabolism processes, such as oxidative phosphorylation and lipid metabolism. Furthermore, NADH: ubiquinone oxidoreductase subunit S4, an important component of the mitochondrial respiratory chain, was increased after AAC and then reversed by EGCG, which was consistent with the proteomics results. Conclusions: EGCG may correct cardiac systolic dysfunction and prevent cardiac remodeling after heart failure via enhancing the energy metabolism, which provides us with new insights into cardioprotective effects of EGCG related to the energy metabolisms in pressure overload-induced cardiac dysfunction."

基金机构：National Natural Science Foundation of China [81974030]

基金资助正文：Funding This work was supported by National Natural Science Foundation of China (Grant No.81974030) .