LAUSR

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. 3-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 (HE) staining, wheat germ agglutinin (WGA) 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). HE staining revealed cardiomyocyte hypertrophy accompanied by a small amount of inflammatory cell infiltration in the AAC+vehicle group. Results of WGA 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 the 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.