Epigallocatechin gallate attenuates overload‑induced cardiac ECM remodeling via restoring T cell homeostasis.

It has previously been demonstrated that Epigallocatechin gallate (EGCG) has regulatory effects on cellular immunity. The present study explored whether EGCG inhibits the overload‑induced cardiac extracellular matrix (ECM) remodeling through targeting the balance of T cell subpopulations. Sprague‑Dawley rats were subjected to either transverse aortic constriction (TAC) or sham operation. TAC rats were treated with EGCG or valsartan (Val) for 6 weeks. The administration of EGCG or Val ameliorated the overproduction of cardiac collagen, inhibited matrix metalloproteinase (MMP) activity, decreased the expression of tissue inhibitor of MMP‑2, atrial natriuretic peptide and brain natriuretic peptide. EGCG regulated the population of effector T cells and naïve T cells, restored the balance of T helper (Th) cell 17/regulatory T cells, via modulating the downstream regulator signal transducer and activator of transcription (STAT3) and STAT5. Furthermore, the ratio of interferon‑γ/interleukin (IL)‑10 which indicates the balance of Th1/Th2, was restored by the treatments at varying degrees. EGCG and Val administration rescued IL‑7 production, and decreased the level of IL‑15 in TAC rats. EGCG has positive therapeutic potential in inhibiting cardiac ECM remodeling. Regulation of the balance of T lymphocyte subsets may be one of the underlying mechanisms responsible for this effect.