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Gypenoside influnces the progression of atherosclerosis in the ApoE－/－ mouse through mTOR/ULK1 pathway
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1.Key Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications of Liaoning University of Traditional Chinese Medicine, ;2.Translational Medicine Research Center of Traditional Chinese Medicine in Liaoning Province, Liaoning University of Traditional Chinese Medicine, ;3.The Second Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, Shenyang 110847, Liaoning, China)

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    Abstract:

    Aim Based on the mTOR/ULK1 autophagy signaling pathway to discuss the mechanism of gypenoside improving aorta lipid deposition of ApoE－/－ mice. Methods 30 healthy ApoE－/－ mice were randomly divided into the model control group and the gypenoside group, and the simvastatin group, 10 mice in each group. 10 C57bL/6J mice were used as the normal control group. The model control group, the gypenoside group and the simvastatin group were fed with high-fat diet for 4 weeks. The gypenoside group and simvastatin group were treated with gypenoside 2.973 g/(kg·d) and simvastatin 2.275 mg/(kg·d) by gastrogavage for 8 weeks, respectively. The normal control group and the model control group were given by gastrogavage with the normal saline of the same volume. The formation of atherosclerotic plaque of the mice was detected by HE staining, and the blood lipid level was detected by the fully automatic biochemical analyser. The expressions of ULK1, Beclin1, LC3 and p-mTOR proteins were dectected by the Western blot.Results Compared with normal control group, in the model control group, TG, TC and LDLC were significantly increased (P＜0.05), HDLC was significantly decreased (P＜0.05), large atheromatous plaques could be seen in aortic canal, ULK1, Beclin1 and LC3 were significantly decreased (P＜0.01), p-mTOR was significantly increased (P＜0.01). Compared with the model control group, in the gypenoside group and the simvastatin group, TG, TC and LDLC were significantly decreased (P＜0.05), HDLC was significantly increased (P＜0.05), atheromatous plaques in aortic canal were significantly decreased, ULK1, Beclin1 and LC3 were significantly increased (P＜0.01), p-mTOR was significantly decreased (P＜0.01 or P＜0.05). Conclusion Gypenosides could relieve the formation of atherosclerotic plaques and prevent atherosclerosis possibly through regulating the autophagy.

    Reference
    [1] 贾连群, 杨关林, 陈文娜, 等.化瘀祛痰方通过调节ApoE－/－小鼠胆固醇代谢相关基因表达抗动脉粥样硬化.中国动脉硬化杂志, 4,2(1):1-6.
    [2] Mizushima N, Komatsu M.Autophagy:renovation of cells and tissues.Cell, 1,7(4):728-741.
    [3] Tiwari RV, Parajuli P, Sylvester PW.Synergistic anticancer effects of combined γ-tocotrienoland oridonin and treatment is associated with the induction of autophagy.Mol Cell Biochem, 5,8(1/2):123-137.
    [4] Cao B, Fan L, Xiang R.Crosstalk between autophagy and apoptosis in endoplasmic reticulum during atherosclerosis.Acta Biophysica Sinica, 3,9(12):911-918.
    [5] Razani B, Feng C, Coleman T, et al.Autophagy links in-flammasomes to atherosclerotic progression.Cell Metab, 2,5(4):534-544.
    [6] 谭华炳, 贺琴, 赵琴.绞股蓝对动脉粥样硬化形成的拮抗作用.中国全科医学, 7,0(6):476-478.
    [7] 权媛, 钱民章.绞股蓝总甙对高脂诱导动脉粥样硬化大鼠炎性分子表达的影响.中国中西医结合杂志, 0,0(4):403-406.
    [8] 史琳, 赵红, 张璐雅, 等.绞股蓝药理作用的研究进展.药物评价研究, 1,4(2):125-129.
    [9] 雷婧, 许韩婷, 苏洁, 等.不同含量绞股蓝皂苷对高脂血症大鼠血脂的影响.上海中医药大学学报, 4,8(2):60-64.
    [10] 寿迪飞, 卢德赵, 王萍儿, 等.绞股蓝总皂苷调节THP-1巨噬细胞源性泡沫细胞胆固醇平衡的作用机制.浙江中医药大学学报, 1,5(2):297-300.
    [11] Wang Q, Liang B, Shirwany NA, et al.2-deoxy-D-glucose treatment of endothelial cells induces autophagy by reactive oxygen species-mediated activation of the AMP-activated protein kinase.PLoS One, 1,6(2):e17234.
    [12] Zhang YL, Cao YJ, Zhang X, et al.The autophagy-lysosome pathway:a novel mechanism involved in the processing of oxidized LDL in human vascular endothelial cells.Biochem Biophys Res Commun, 0,4(2):377-382.
    [13] Li S, Wang L, Hu Y, et al.Autophagy regulators as potential cancer therapeutic agents:a review.Curr Top Med Chem, 5,5(8):720-744.
    [14] Razani B, Feng C, Coleman T, et al.Autophagy links inflammasomes to atherosclerotic progression.Cell Metab, 2,5(4):534-544.
    [15] Kim J, Kundu M, Viollet B, et al.AMPK and mTOR regulate autophagy through direct phosphorylation of ULK1.Nat Cell Biol, 1,3(2):132-141.
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SONG Nan, YANG Fang, CAO Hui-Min, ZHANG Ni, JIA Lian-Qun, CHEN Wen-Na, YANG Guan-Lin. Gypenoside influnces the progression of atherosclerosis in the ApoE－/－ mouse through mTOR/ULK1 pathway[J]. Editorial Office of Chinese Journal of Arteriosclerosis,2018,26(2):127-132.

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History
  • Received:July 14,2017
  • Revised:August 20,2017
  • Online: March 07,2018
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