中国病理生理杂志2018，Vol.34Issue(5)：832-838,7.DOI:10.3969/j.issn.1000-4718.2018.05.010
山柰酚-3-O-芸香糖苷对血管平滑肌细胞增殖、迁移及TGFBR1信号通路活化的影响
Effects of kaempferol-3-O-rutinoside on proliferation,migration and TG-FBR1 signaling pathway activation in vascular smooth muscle cells
摘要
Abstract
AIM:To investigate the effects of kaempferol-3-O-rutinoside(KR)on the proliferation,migration of vascular smooth muscle cells(VSMC)and the activation of transforming growth factor βreceptor 1(TGFBR1)signaling pathway in the cells.METHODS: The viability of VSMC was detected by MTT assay.The proliferation of VSMC was measured by EdU staining.The migration ability of VSMC was examined by Transwell assay.The protein levels of the mi-gration-associated proteins matrix metalloproteinase 2(MMP2)and matrix metalloproteinase 9(MMP9)were detected by Western blot.Molecular docking study was conducted to explore the interaction between KR and TGFBR 1.The protein le-vels of the phosphorylated TGFBR1,Smad2 and Smad3 were determined by Western blot.RESULTS: KR inhibited the viability of VSMC in a dose-and time-dependent manner.KR reduced the ratio of EdU-positive cells in a dose-dependent manner.KR dose-dependently suppressed the migration ability of VSMC and decreased the protein levels of MMP 2 and MMP9(P<0.05).KR docked into TGFBR1 with the binding energy of -9.804 kcal/mol by forming hydrogen bonds with SER-280,ARG-215,ASP-290 and LYS-335 of TGBFR1.KR dose-dependently suppressed the activation of TGFBR 1 and its downstream proteins Smad2 and Smad3(P<0.05).CONCLUSION: KR inhibits the proliferation and migration of VSMC,possibly via blocking the TGFBR1 signaling pathway.关键词
山柰酚-3-O-芸香糖苷/血管平滑肌细胞/细胞增殖/细胞迁移/TGFBR1信号通路Key words
Kaempferol-3-O-rutinoside/Vascular smooth muscle cells/Cell proliferation/Cell migration/TGFBR1 signaling pathway分类
医药卫生引用本文复制引用
张文通,李俊,吴玉婷,范慧婕,谢凌鹏,谭章斌,毕艺鸣,刘彬,周迎春..山柰酚-3-O-芸香糖苷对血管平滑肌细胞增殖、迁移及TGFBR1信号通路活化的影响[J].中国病理生理杂志,2018,34(5):832-838,7.基金项目
国家自然科学基金资助项目(No.81373575 （）
No.81673805) （）
广东省科技计划(No.2016A020226026) （No.2016A020226026）
广东省中医药局资助项目(No.20161167) （No.20161167）
