College of Life Science, Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China.
College of Basic Medicine, Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China.
Sci Rep. 2022 Feb 1;12(1):1708. doi: 10.1038/s41598-022-05804-9.
Numerous studies have demonstrated that endothelial cell senescence plays a decisive role in the development and progression of cardiovascular diseases (CVD). Our previous results confirmed that Tetrahydroxy stilbene glycoside (TSG) can alleviate the human umbilical vein endothelial cells (HUVECs) senescence induced by HO through SIRT1. It has been reported that miR-34a is a translational suppressor of SIRT1. In this study, we aimed to explore whether TSG regulates SIRT1 through miR-34a to ameliorate HUVECs senescence. HO was used to induce premature senescence in HUVECs, and miR-34a mimic or inhibitor were transfected to over-express or suppress the expression level of miR-34a. Results revealed that TSG apparently decreased the miR-34a expression level in HO-induced premature senescence of HUVECs. When SIRT1 expression was inhibited by EX527, the attenuation of TSG on the expression level of miR-34a were abolished. When miR-34a expression was knockdown, the effect of TSG on HUVECs senescence could be enhanced. While miR-34a mimic could reverse the effect of TSG on HUVECs senescence. In conclusion, we demonstrated that TSG could attenuated endothelial cell senescence by targeting miR-34a/SIRT1 pathway.
大量研究表明内皮细胞衰老在心血管疾病（CVD）的发生和发展中起决定性作用。我们之前的研究结果证实二苯乙烯苷（TSG）可通过 SIRT1 减轻 HO 诱导的人脐静脉内皮细胞（HUVEC）衰老。有报道称 miR-34a 是 SIRT1 的翻译抑制剂。本研究旨在探讨 TSG 是否通过 miR-34a 调节 SIRT1 来改善 HUVEC 衰老。HO 用于诱导 HUVEC 过早衰老，转染 miR-34a 模拟物或抑制剂以过表达或抑制 miR-34a 的表达水平。结果表明，TSG 明显降低了 HO 诱导的 HUVEC 过早衰老中 miR-34a 的表达水平。当 SIRT1 表达被 EX527 抑制时，TSG 对 miR-34a 表达水平的衰减作用被消除。当 miR-34a 表达被敲低时，TSG 对 HUVEC 衰老的作用可以增强。而 miR-34a 模拟物可以逆转 TSG 对 HUVEC 衰老的作用。综上所述，我们证明了 TSG 可以通过靶向 miR-34a/SIRT1 通路来减轻内皮细胞衰老。
