Secondary Logo

Journal Logo

Institutional members access full text with Ovid®

Ameliorative Effect of Epigallocatechin Gallate on Cardiac Hypertrophy and Fibrosis in Aged Rats

Muhammed, Ibrahim PhD*; Sankar, Suruthi MSc*; Govindaraj, Sakthivel MSc

Erratum

In the article that appeared on pages 65 to 75 of the February 2018 issue of Journal of Cardiovascular Pharmacology , figure 2A was incorrect. The correct figure 2A is below:

Journal of Cardiovascular Pharmacology. 71(5):324, May 2018.

Journal of Cardiovascular Pharmacology: February 2018 - Volume 71 - Issue 2 - p 65–75
doi: 10.1097/FJC.0000000000000545
Original Article
Buy
Erratum

Abstract: The objective of the present study is to evaluate the effect of epigallocatechin gallate (EGCG) on aging-mediated cardiac hypertrophy, fibrosis, and apoptosis. The Wistar albino rats were divided into 4 groups (n = 18). Group I: young (3 months), group II: aged (24–26 months), group III: aged + EGCG (200 mg/kg for 30 days), and group IV: young + EGCG. At the end of 30 days, EGCG administration to the aged animals showed significant (P < 0.001) reduction of low-density lipoprotein, very low-density lipoprotein, triglyceride, total cholesterol with concomitant increase of high-density lipoprotein (P < 0.001) when compared with aged rats. Increased (P < 0.001) heart volume, weight with concomitant increase of left ventricular wall thickness, and reduced ventricular cavity were observed in aged rats supplemented with EGCG compared with aged animals. Histology and histomorphometry study of aged animals treated with EGCG showed marked increases in the diameter and volume of cardiomyocytes with concomitant reduction of numerical density when compared with aged animals. Reduced reactive oxygen species (P < 0.001) production with association of increased antioxidant defense system (P < 0.001) in aged hearts supplemented with EGCG when compared with aged animals. TUNEL staining and fibrosis showed a marked increase in apoptotic cell death (P < 0.001) and collagen deposition (P < 0.001) in aged animals treated with EGCG when compared with aged animals. Aged animals treated with EGCG showed a marked increase in protein expression of TGFβ, TNFα, and nuclear factor kappa B (NF-κB) and significant (P < 0.001) alteration in the gene expression of TGFβ, TNFα, NF-κB, α-SMA, and Nrf2 when compared with aged animals. Taken together, it is evident that EGCG may potentially inhibit aging-induced cardiac hypertrophy, fibrosis, and apoptosis, thereby preserving cardiac function. The proposed mechanism would be inhibition of reactive oxygen species–dependent activation of TGFβ1, TNFα, and NF-κB signaling pathway. Hence, the present study suggests that EGCG can be useful to fight against aging-induced cardiac hypertrophy, fibrosis, and apoptosis.

Departments of *Anatomy; and

Physiology, Dr. ALM Postgraduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai, India.

Reprints: Ibrahim Muhammed, PhD, Department of Anatomy, Dr. ALM Postgraduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600 113, India (e-mail: ibrahimm8411@gmail.com).

This work was performed under the financial assistance of Science and Engineering Research Board—Department of Science and Technology, Government of India (Grant No. SERB/F/4412/2013-14).

The authors report no conflicts of interest.

Received April 11, 2017

Accepted September 29, 2017

Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.