Treg/Th17 Ratio Regulation May Play an Important Role in Epigallocatechin-3-Gallate–Mediated Attenuation of Increased Afterload-Induced Cardiac Hypertrophy. Issue 5 (20th May 2022)

• Record Type: Journal Article
• Authors: Luo, Min; Mou, Qiuhong; Liu, Lingjuan; Tian, Jie; Liu, Lifei
• Is Part Of: Journal of cardiovascular pharmacology. Volume 79:Issue 5(2022)
• Page Start: 711
• Page End: 718
• Publication Date: 2022-05-20
• Subjects: cardiac hypertrophy -- epigallocatechin-3-gallate -- increased afterload -- Treg -- Th17; Cardiovascular Diseases -- drug therapy -- Periodicals; Cardiovascular System -- drug effects -- Periodicals; Cardiovascular pharmacology -- Periodicals; Cardiovascular agents -- Periodicals; Cardiovascular agents; Cardiovascular pharmacology; Periodicals; 615.7105
• DOI: 10.1097/FJC.0000000000001220
• Languages: English
• ISSNs: 0160-2446

Abstract

Abstract: The aim of this study was to investigate whether Treg/Th17 ratio regulation plays an important role in epigallocatechin-3-gallate (EGCG) in attenuating increased afterload-induced cardiac hypertrophy. Three-month-old male C57BL/6 mice were divided into sham + vehicle, abdominal aortic constriction (AAC) + vehicle, and AAC + EGCG groups. Intraperitoneal EGCG (50 mg/kg/d) administration was conducted. Cardiac structure and function were examined by ultrasonography. Pathology was examined by hematoxylin and eosin staining, wheat germ agglutinin staining, and Masson's trichome staining. T-lymphocyte subtypes were analyzed using immunofluorescence and flow cytometry assays. Ultrasonography showed that the ventricular wall in the AAC + vehicle group was thicker than that in the sham + vehicle group ( P < 0.05). Hematoxylin and eosin staining revealed cardiomyocyte hypertrophy accompanied by a small amount of inflammatory cell infiltration in the AAC + vehicle group. The results of wheat germ agglutinin staining demonstrated the presence of hypertrophic cardiomyocytes in the AAC + vehicle group ( P < 0.01). Masson's trichome staining showed cardiac fibrosis in the AAC + vehicle group, and the immunofluorescence assay revealed infiltration of CD4 + cells in both AAC + vehicle and AAC + EGCG groups. Splenic flow cytometry showed a significant increase in the proportion of Treg cells in the AAC + EGCG group ( P < 0.05). The proportion of Th17 cells in the AAC + vehicle group was significantly higher than that in the sham + vehicle group ( P < 0.05). In conclusion, changes in the Treg/Th17 ratio are associated with the occurrence of myocardial hypertrophy caused by increased afterload. Moreover, regulation of the Treg/Th17 ratio by EGCG may play an important role in the attenuation of myocardial hypertrophy.