Abstract | CONTEXT: 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.
|
Authors | Yue Cui, Yongqiang Wang, Gang Liu |
Journal | Pharmaceutical biology
(Pharm Biol)
Vol. 59
Issue 1
Pg. 1305-1313
(Dec 2021)
ISSN: 1744-5116 [Electronic] England |
PMID | 34607503
(Publication Type: Journal Article)
|
Chemical References |
- Cardiotonic Agents
- Catechin
- epigallocatechin gallate
- mTOR protein, mouse
- Proto-Oncogene Proteins c-akt
- TOR Serine-Threonine Kinases
|
Topics |
- Animals
- Cardiomegaly
(prevention & control)
- Cardiotonic Agents
(administration & dosage, pharmacology)
- Catechin
(administration & dosage, analogs & derivatives, pharmacology)
- Disease Models, Animal
- Dose-Response Relationship, Drug
- Fibrosis
(prevention & control)
- Male
- Mice
- Mice, Inbred C57BL
- Proto-Oncogene Proteins c-akt
(metabolism)
- TOR Serine-Threonine Kinases
(metabolism)
|