Icariside II Attenuates Vascular Remodeling Via Wnt7b/CCND1 Axis

Icariside II Attenuates Vascular Remodeling Via Wnt7b/CCND1 Axis
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DOI:
10.1097/fjc.0000000000001239
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发表时间:
2022-02
影响因子:
3
通讯作者:
Hong-Yu Wu;Jiayan Li;Hao Wen;Yi-qi Li;Ye-li Li;Guang Li;Yanmeng Jiang;Junyuan Lv;Dan-li Yang
Hong-Yu Wu;Jiayan Li;Hao Wen;Yi-qi Li;Ye-li Li;Guang Li;Yanmeng Jiang;Junyuan Lv;Dan-li Yang
中科院分区:
医学4区
文献类型:
--
作者:
Hong-Yu Wu;Jiayan Li;Hao Wen;Yi-qi Li;Ye-li Li;Guang Li;Yanmeng Jiang;Junyuan Lv;Dan-li Yang

文献摘要

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翻译后摘要:血管成形术往往失败,由于血管平滑肌细胞(VSMCs)的异常增殖。血管成形术的成功率可能会增加后,管理剂,有效地改善异常血管重塑。淫羊藿苷II(ICS-II)是从中草药淫羊藿中提取的天然黄酮醇糖苷,具有多种对人类有益的药用品质。尽管如此,ICS-II在解决异常血管重塑中的作用仍有待澄清。本研究探讨了ICS-Ⅱ对大鼠球囊损伤后内膜增生和血小板源性生长因子(PDGF)诱导的大鼠主动脉平滑肌细胞(VSMCs)增殖的影响。发现ICS-II与本研究中使用的阳性对照雷帕霉素一样有效。ICS-II抑制大鼠颈动脉损伤后新生内膜的形成,并显著降低Wnt 7 b的表达。ICS-Ⅱ可显著抑制血小板源性生长因子诱导的VSMCs增殖。细胞周期分析显示ICS-II在G1/S转换期间触发细胞周期阻滞。Western印迹分析进一步表明,这种细胞周期阻滞可能是通过Wnt 7 b抑制导致CCND 1抑制。总之,我们的研究结果表明,ICS-II具有显着的抗增殖素质,抵消异常血管新生内膜增生。这种现象很可能是由于Wnt 7 b/CCND 1轴的抑制而发生的。
Abstract: Angioplasty often fails due to the abnormal proliferation of vascular smooth muscle cells (VSMCs). Success rates of angioplasty may increase following the administration of an agent that effectively ameliorates aberrant vascular remodeling. Icariside II (ICS-II) is a natural flavonol glycoside extract from the Chinese herbal medicine Epimedii that possesses several medicinal qualities that are beneficial in humans. Nevertheless, the role of ICS-II in addressing aberrant vascular remodeling have yet to be clarified. The current investigation studies the molecular effects of ICS-Ⅱ on balloon-inflicted neointimal hyperplasia in rats in vivo and on platelet-derived growth factor–induced vascular proliferation in primary rat aortic smooth muscle cells (VSMCs) in vitro. ICS-II was found to be as effective as rapamycin, the positive control used in this study. ICS-II inhibited neointimal formation in injured rat carotid arteries and notably reduced the expression of Wnt7b. ICS-Ⅱ significantly counteracted platelet-derived growth factor–induced VSMCs proliferation. Cell cycle analysis showed that ICS-II triggered cell cycle arrest during the G1/S transition. Western blot analysis further indicated that this cell cycle arrest was likely through Wnt7b suppression that led to CCND1 inhibition. In conclusion, our findings demonstrate that ICS-II possesses significant antiproliferative qualities that counteracts aberrant vascular neointimal hyperplasia. This phenomenon most likely occurs due to the suppression of the Wnt7b/CCND1 axis.