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总皂苷抑制球囊损伤诱导的大鼠颈动脉内膜增生。

Total Ginsenosides suppress the neointimal hyperplasia of rat carotid artery induced by balloon injury.

机构信息

Department of pharmacology, Zunyi Medical College, Zunyi, 563000, PR China.

出版信息

Vascul Pharmacol. 2011 Jan-Feb;54(1-2):52-7. doi: 10.1016/j.vph.2010.12.003. Epub 2010 Dec 25.

DOI:10.1016/j.vph.2010.12.003
PMID:21187161
Abstract

Ginsenosides, the active components found in Panax ginseng, have been reported to inhibit the cardiac hypertrophy in rats. This study aims to observe the potential effect of total ginsenosides (TG) on the hypertrophic vascular diseases. The model of vascular neointimal hyperplasia was established by rubbing the endothelia of the common carotid artery with a balloon in male Sprague Dawley rats. TG (15 mg/kg/day, 45 mg/kg/day), L-arginine (L-arg) 200 mg/kg/day, and NG-nitro-L-arginine-methyl ester (L-NAME) 100 mg/kg/day used with the same dose of L-arg or TG 45 mg/kg/day were given for 7 and 14 consecutive days after surgery. TG and L-arg administrations significantly ameliorated the histopathology of injured carotid artery, which was abolished or blunted by L-NAME, an NOS inhibitor; TG and L-arg could also remarkably reduce the expression of proliferating cell nuclear antigen (PCNA), a proliferation marker of vascular smooth muscle cells(VSMCs), in neointima of the injured artery wall. Further study indicated that balloon injury caused a decreased superoxide dismutase (SOD) activity and an elevated malondialdehyde (MDA) content in plasma, and reduced the cGMP level in the artery wall, which were reversed by TG. It was concluded that TG suppress the rat carotid artery neointimal hyperplasia induced by balloon injury, which may be involved in its anti-oxidative action and enhancing the inhibition effects of NO/cGMP on VSMC proliferation.

摘要

人参中的活性成分——人参皂苷已被报道可抑制大鼠的心肌肥厚。本研究旨在观察总人参皂苷(TG)对血管肥厚性疾病的潜在作用。通过用球囊摩擦雄性 Sprague Dawley 大鼠颈总动脉内皮,建立血管新生内膜增生模型。在手术后连续 7 天和 14 天,给予 TG(15mg/kg/天、45mg/kg/天)、L-精氨酸(L-arg)200mg/kg/天和 NG-硝基-L-精氨酸甲酯(L-NAME)100mg/kg/天,并用相同剂量的 L-arg 或 TG 45mg/kg/天进行治疗。NOS 抑制剂 L-NAME 可消除或减弱 TG 和 L-arg 对损伤颈动脉组织病理学的改善作用;TG 和 L-arg 还可显著降低损伤动脉壁内膜中增殖细胞核抗原(PCNA)的表达,PCNA 是血管平滑肌细胞(VSMCs)的增殖标志物。进一步的研究表明,球囊损伤导致血浆中超氧化物歧化酶(SOD)活性降低和丙二醛(MDA)含量升高,并降低了动脉壁中环鸟苷酸(cGMP)的水平,而 TG 可逆转这些变化。总之,TG 抑制了球囊损伤引起的大鼠颈总动脉新生内膜增生,这可能与其抗氧化作用和增强 NO/cGMP 对 VSMC 增殖的抑制作用有关。

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