Ginsenoside Re inhibits vascular neointimal hyperplasia in balloon-injured carotid arteries through activating the eNOS/NO/cGMP pathway in rats
Ginsenoside Re inhibits vascular neointimal hyperplasia in balloon-injured carotid arteries through activating the eNOS/NO/cGMP pathway in rats
复制标题
人参皂苷 Re 通过激活 eNOS/NO/cGMP 通路抑制大鼠球囊损伤颈动脉血管新生内膜增生
DOI：
10.1016/j.biopha.2018.07.044
复制
发表时间：
2018-10-01
影响因子：
7.5
通讯作者：
Yang, Dan-Li
中科院分区：
文献类型：
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作者：
Gao, Yang;Gao, Chen-Ying;Yang, Dan-Li
人参皂苷Re(GS-Re)是著名的中药人参的主要成分之一，具有多种有益作用，包括血管松弛、抗氧化、抗炎和抗癌特性。本研究的目的是观察GS-Re对球囊损伤诱导的动脉内膜增生的影响，并探讨其作用机制。采用球囊摩擦大鼠颈总动脉(CCA)内皮细胞的方法建立大鼠颈总动脉(CCA)血管新生内膜增生模型，然后给予GS-Re(12.5、25、50 mg/kg/d)连续灌胃14d。经GS-Re处理后，GS-Re 25.0和50.0 mg/kg/d(中、高剂量)组损伤血管管腔明显增加。此外，中、高剂量组增殖细胞核抗原阳性细胞百分率降低，SMα-肌动蛋白阳性细胞数增加，NO、cGMP、enos mRNA水平及PHOS-eNOS(Ser1177)/enos蛋白比值明显升高。此外，L能不同程度地阻断GS-Re对NO和eNOS表达的促进作用。提示GS-Re可通过抑制VSMC增殖抑制球囊损伤诱导的血管内膜增生，其机制与激活eNOS/NO/cGMP通路密切相关。
Ginsenoside Re (GS-Re) is one of the main ingredients of ginseng, a widely known Chinese traditional medicine, and has a variety of beneficial effects, including vasorelaxation, antioxidative, anti-inflammatory, and anticancer properties. The aims of the present study were to observe the effect of GS-Re on balloon injury-induced neointimal hyperplasia in the arteries and to investigate the mechanisms underlying this effect. A rat vascular neointimal hyperplasia model was generated by rubbing the endothelium of the common carotid artery (CCA) with a balloon, and GS-Re (12.5, 25 or 50 mg/kg/d) were subsequently continuously administered to the rats by gavage for 14 days. After GS-Re treatment, the vessel lumen of injured vessels showed significant increases in the GS-Re 25.0 and 50.0 mg/kg/d (intermediate- and high-dose) groups according to H.E. staining. Additionally, a reduced percentage of proliferating cell nuclear antigen (PCNA)-positive cells and an increased number of SM alpha-actin-positive cells were detected, and the levels of NO, cyclic guanosine monophosphate (cGMP), and eNOS mRNA as well as the phos-eNOS(ser1177)/eNOS protein ratio were obviously upregulated in the intermediate- and high-dose groups. Moreover, the promotive effects of GS-Re on NO and eNOS expression were blocked by L-NAME treatment to different degrees. These results suggested that GS-Re can suppress balloon injury-induced vascular neointimal hyperplasia by inhibiting VSMC proliferation, which is closely related to the activation of the eNOS/NO/cGMP pathway.