Notoginsenoside R1 attenuates atherosclerotic lesions in ApoE deficient mouse model.
Notoginsenoside R1 attenuates atherosclerotic lesions in ApoE deficient mouse model.
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三七皂苷 R1 减轻 ApoE 缺陷小鼠模型中的动脉粥样硬化病变
DOI：
10.1371/journal.pone.0099849
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Zhang T
中科院分区：
文献类型：
--
作者：
Jia C;Xiong M;Wang P;Cui J;Du X;Yang Q;Wang W;Chen Y;Zhang T
动脉粥样硬化是心血管疾病和中风的主要原因。本研究评价了天然化合物三七皂苷R1对载脂蛋白E−/−小鼠动脉粥样硬化的干预作用。NR1治疗显著减轻了动脉粥样硬化病变，这种缓解通过减少脂肪沉积、纤维化和氧化应激而显著。−/−组小鼠血清谷胱甘肽和超氧化物歧化酶水平升高，丙二醛水平降低。NR1治疗还能显著降低CHO、TG、OX-LDL水平，升高高密度脂蛋白水平。此外，IL-2、IL-6、肿瘤坏死因子-α和γ-干扰素等炎性细胞因子水平显著降低。此外，载脂蛋白E−/−组小鼠主动脉miR-26a、miR-21、miR-126a、miR-132、miR-146和miR-155的表达显著增加，miR-20a和miR-92a的表达显著降低。而NR1处理后，miR-21、miR-26a、miR-126的表达显著降低，miR-20a的表达显著增加。总之，我们的结果首次证明了NR1的抗动脉粥样硬化作用，这可能部分是通过其对炎症、氧化应激、脂代谢和microRNA表达的多重靶向作用来介导的。因此，这些结果证明了进一步评价NR1作为治疗动脉粥样硬化的药物的合理性。
Atherosclerosis is the primary cause of cardiovascular diseases and stroke. The current study evaluated the interventional effects of a naturally occurring compound Notoginsenoside R1 (NR1) on atherosclerosis in ApoE−/− mice. The atherosclerotic lesion was significantly alleviated by NR1 treatment and this attenuation was marked by reduction in lipid deposition, fibrosis and oxidative stress. Increased serum levels of GSH and SOD and decreased level of MDH were observed in NR1-treated ApoE−/− mice. NR1 treatment also significantly decreased the levels of CHO, TG, ox-LDL and increased the level of HDL. Additionally, the levels of inflammatory cytokines including IL-2, IL-6, TNF-α and γ-IFN were markedly reduced in NR1-treated ApoE−/− mice. Furthermore, significantly increased aortic expression of miR-26a, miR-21, miR-126a, miR-132, miR-146 and miR-155 and decreased expression of miR-20a and miR-92a were observed in the vehicle-treated ApoE−/− mice. While NR1 treatment led to a significant reduction in the expression of miR-21, miR-26a, miR-126 and increased expression of miR-20a. Collectively, our results demonstrated for the first time the anti-atherosclerotic effects of NR1, which could be in part mediated through its multiple targeting effects on inflammation, oxidative stress, lipid metabolism and microRNA expression. These results therefore justify further evaluation of NR1 as a therapeutic agent treating atherosclerosis.
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