Medical College of Wuhan University of Science and Technology, Wuhan, 430081, China.
Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Curr Med Sci. 2022 Oct;42(5):981-990. doi: 10.1007/s11596-022-2604-6. Epub 2022 Jul 27.
Epidemiology studies indicate that green tea polyphenols (GTP) perform a protective effect on cardiovascular diseases, but the underlying mechanisms are complex. The present study aimed to investigate the effect of GTP on high-fat diets (HFD) induced-early vascular aging.
Six-week young adult Wistar rats were fed with standard chow or HFD in the presence and absence of GTP (200 mg/kg body weight) for 18 weeks. In vitro experiment, human umbilical vascular endothelial cells (HUVECs) were treated with palmitic acid (PA) and GTP.
The results showed that GTP alleviated the disorganized arterial wall and the increased intima-media thickness induced by HFD. In addition, the vascular oxidative injury was suppressed following GTP treatment. Furthermore, GTP elevated the ratio of LC3-II/LC3-I and suppressed expression of p62/SQSTM1, and restored SIRT3 expression in the aorta of HFD rats. Consistently, in cultured HUVECs, GTP inhibited cell senescence indicated by SA-β-gal and promoted endothelial autophagy compared with the PA treatment group. The activity of SIRT3 was specifically inhibited by 3-TYP, and the protective effect of GTP was consequently abolished.
The findings indicated that GTP protected against early vascular senescence in young HFD rats via ameliorating oxidative injury and promoting autophagy which was partially regulated by the SIRT3 pathway.
流行病学研究表明，绿茶多酚（GTP）对心血管疾病具有保护作用，但作用机制复杂。本研究旨在探讨 GTP 对高脂肪饮食（HFD）诱导的早期血管衰老的影响。
6 周龄成年 Wistar 大鼠分别给予标准饲料或 HFD，并分别给予或不给予 GTP（200mg/kg 体重）喂养 18 周。体外实验中，用人脐静脉内皮细胞（HUVEC）处理棕榈酸（PA）和 GTP。
结果表明，GTP 缓解了 HFD 引起的动脉壁排列紊乱和内膜-中膜厚度增加。此外，GTP 处理抑制了血管氧化损伤。此外，GTP 增加了 LC3-II/LC3-I 的比值，并抑制了 HFD 大鼠主动脉中 p62/SQSTM1 的表达，恢复了 SIRT3 的表达。在培养的 HUVEC 中，与 PA 处理组相比，GTP 抑制了 SA-β-gal 所示的细胞衰老，并促进了内皮细胞自噬。SIRT3 的活性被 3-TYP 特异性抑制，GTP 的保护作用因此被消除。
这些发现表明，GTP 通过改善氧化损伤和促进自噬来预防年轻 HFD 大鼠的早期血管衰老，部分受 SIRT3 途径调节。
