Epigallocatechin gallate (EGCG) attenuates myocardial hypertrophy and fibrosis induced by transverse aortic constriction via inhibiting the Akt/mTOR pathway.

contextEpigallocatechin gallate (EGCG) is the most abundant catechin from tea. Previous studies have indicated EGCG has a cardioprotective effect.

objectiveThis manuscript mainly explores the role of EGCG in pressure-overload cardiac hypertrophy and its mechanism related to the Akt/mTOR pathway. METHODS AND

methodsTransverse aortic constriction (TAC) was utilized to establish the cardiac hypertrophy mice model. C57BL/6 mice were assigned into 6 groups. Starting from the first day after surgery, mice received different doses of EGCG (20, 40, 80 mg/kg) or vehicle orally for four weeks. Heart weight to body weight (HW/BW) ratio and heart weight to tibia length (HW/TL) ratio as well as hematoxylin-eosin staining were utilized to evaluate cardiac hypertrophy. Masson's trichrome and Sirius red staining were used to depict cardiac fibrosis. The expressions of fibrosis and hypertrophy-related markers and Akt/mTOR pathway were quantified by western blot and qRT-PCR.

resultsEGCG significantly attenuated cardiac function shown by decreased HW/BW (TAC, 6.82 ± 0.44 vs. 20 mg/kg EGCG, 5.53 ± 0.45; 40 mg/kg EGCG, 4.79 ± 0.32; 80 mg/kg EGCG, 4.81 ± 0.38) and HW/TL (TAC, 11.94 ± 0.69 vs. 20 mg/kg EGCG, 11.44 ± 0.49; 40 mg/kg EGCG, 8.83 ± 0.58; 80 mg/kg EGCG, 8.98 ± 0.63) ratios as well as alleviated cardiac histology. After treatment, hemodynamics was improved, cardiac fibrosis was attenuated. The activated Akt/mTOR pathway was inhibited by EGCG. DISCUSSION AND

conclusionsEGCG plays a protective role in the TAC model by regulating the Akt/mTOR pathway, which provides a theoretical basis for its clinical treatment.