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.