Key result
Epigallocatechin gallate reduces cardiac hypertrophy in mice, lowering heart-to-body weight ratio ~30% after TAC.
Why the study?
Previous studies indicated epigallocatechin gallate has a cardioprotective effect, but its role and Akt/mTOR pathway mechanism in pressure-overload cardiac hypertrophy remained to be explored.
Does oral epigallocatechin gallate (EGCG) attenuate myocardial hypertrophy and fibrosis in mice with transverse aortic constriction-induced pressure overload?
Does oral epigallocatechin gallate (EGCG) attenuate myocardial hypertrophy and fibrosis in mice with transverse aortic constriction-induced pressure overload?
In a murine pressure-overload model, oral EGCG attenuated myocardial hypertrophy and cardiac fibrosis and improved hemodynamics via inhibition of the Akt/mTOR signaling pathway.
Answers are grounded in this paper and cite their sources.
Attenuates hypertrophy in TAC mice; leaves open human translation and requires clinical trials.
CONTEXT: Epigallocatechin gallate (EGCG) is the most abundant catechin from tea. Previous studies have indicated EGCG has a cardioprotective effect. OBJECTIVE: This manuscript mainly explores the role of EGCG in pressure-overload cardiac hypertrophy and its mechanism related to the Akt/mTOR pathway. METHODS AND METHODS: Transverse 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. RESULTS: EGCG 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 CONCLUSIONS: EGCG plays a protective role in the TAC model by regulating the Akt/mTOR pathway, which provides a theoretical basis for its clinical treatment.
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Cui et al. (2021) studied Pressure-overload cardiac hypertrophy and fibrosis induced by transverse aortic constriction (TAC) (n=120). Epigallocatechin gallate (EGCG) vs. Vehicle control (alongside sham and normal control groups) was evaluated on Heart weight to body weight (HW/BW) ratio (mg/g) at 4 weeks (40 mg/kg EGCG vs. TAC vehicle control) (p=<0.01). Epigallocatechin gallate (40 mg/kg) reduced the heart weight to body weight ratio to 4.79 ± 0.32 mg/g compared to 6.82 ± 0.44 mg/g in TAC mice (p < 0.01).
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