表没食子儿茶素没食子酸酯通过 CaN-NFAT 信号通路在血管紧张素 II 诱导的病理性心肌肥厚中的预防作用。

The Prevention Role of Theaflavin-3,3'-digallate in Angiotensin II Induced Pathological Cardiac Hypertrophy via CaN-NFAT Signal Pathway.

机构信息

Department of Tea Science, Zhejiang University, Hangzhou 310058, China.

College of Tea Science, Yunnan Agricultural University, Kunming 650201, China.

出版信息

Nutrients. 2022 Mar 26;14(7):1391. doi: 10.3390/nu14071391.

Theaflavin-3,3'-digallate (TF3) is a representative theaflavin of black tea and is remarkable for the anti-coronary heart disease effect. As an adaptive response to heart failure, pathological cardiac hypertrophy (PCH) has attracted great interest. In this study, the PCH cell model was established with H9c2 cells by angiotensin II, and the prevention effect and mechanisms of TF3 were investigated. The results showed that the cell size and fetal gene mRNA level were significantly reduced as pretreated with TF3 at the concentration range of 1-10 μM, also the balance of the redox system was recovered by TF3 at the concentration of 10 μM. The intracellular Ca level decreased, Calcineurin (CaN) expression was down-regulated and the p-NFATc3 expression was up-regulated. These results indicated that TF3 could inhibit the activation of the CaN-NFAT signal pathway to prevent PCH, and TF3 may be a potentially effective natural compound for PCH and heart failure.

茶黄素-3,3′-二没食子酸酯（TF3）是红茶中一种具有代表性的茶黄素，具有抗冠心病的作用。病理性心肌肥厚（PCH）作为心力衰竭的一种适应性反应，引起了广泛关注。本研究以血管紧张素Ⅱ诱导 H9c2 细胞建立 PCH 细胞模型，探讨 TF3 的防治作用及机制。结果表明，TF3 在 1-10 μM 浓度范围内预处理可显著减小细胞体积，降低胎儿基因 mRNA 水平，同时 10 μM 的 TF3 可恢复氧化还原系统的平衡。细胞内 Ca 水平降低，钙调神经磷酸酶（CaN）表达下调，p-NFATc3 表达上调。这些结果表明，TF3 可抑制 CaN-NFAT 信号通路的激活，从而预防 PCH，TF3 可能是一种治疗 PCH 和心力衰竭的潜在有效天然化合物。