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仙茅苷对脂多糖诱导血管平滑肌细胞增殖、迁移及表型转化的影响 被引量:1

Effects of curculigoside on the proliferation,migration and phenotypic transformation of lipopolysaccharide-induced vascular smooth muscle cell
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摘要 目的观察仙茅苷(curculigoside,Cur)对脂多糖(LPS)诱导血管平滑肌细胞(vascular smooth muscle cells,VSMCs)发生细胞增殖、迁移以及促进其表型转化的影响,并对其机制进行初步探讨。方法体外分离培养大鼠血管平滑肌细胞,将血管平滑肌细胞随机分为对照组、脂多糖组、脂多糖+不同浓度仙茅苷组及仙茅苷组。采用噻唑蓝(MTT)比色法观察并计算各组细胞增殖率;采用细胞划痕实验观察并计算细胞迁移率。应用Western blot法检测各组细胞内α-平滑肌肌动蛋白(α-SMA)、基质金属蛋白酶9(MMP-9)及核转录因子κB(NF-κB)信号通路相关蛋白表达情况。结果与对照组相比,脂多糖组细胞增殖率、迁移率及细胞内核转录因子κB及基质金属蛋白酶9蛋白表达水平明显提高(P<0.001),而α-平滑肌肌动蛋白表达明显降低(P<0.001);与脂多糖组相比,脂多糖+仙茅苷组细胞增殖率、迁移率以及细胞内基质金属蛋白酶9、核转录因子κB蛋白表达水平明显下降(P<0.001),α-平滑肌肌动蛋白表达水平明显上升(P<0.001)。结论仙茅苷可明显抑制由脂多糖诱导的血管平滑肌细胞表型自收缩表型向合成表型转化,进而抑制血管平滑肌细胞的增殖与迁移能力。其作用机制可能与核转录因子κB信号通路相关。 Objective To investigate curculigoside on the proliferation,migration and phenotypic transformation of LPS-induced vascular smooth muscle cell.Methods Vascular smooth muscle cells(VSMC)were obtained from rat thoracic aorta,and then randomly divided into control group,LPS,LPS+Cur group and Cur group.MTT was used to detected the effects of Cur on proliferation of VSMCs;The cell scratch test was used to detected the effects of Cur on cell migration;The indicator were detected by Western blot,which included the expression level ofα-SMA,MMP-9 and NF-κB.Results Compared with control group,the proliferation inhibitory and migration rates of cells after treatment with LPS for 24 h were significantly increased(P<0.001),and the expression of NF-κB and MMP-9 protein of cells after treatment with Cur for 24 h were significantly up-regulated,while the expression ofα-SMA decreased(P<0.001).After adding Cur,the proliferation inhibitory and migration rates were lower than these of LPS group,and the expression of MMP-9 and NF-κB was lower than that of the LPS group,and theα-SMA protein expression increased(P<0.001).Conclusion Cur can inhibit the proliferation,migration and phenotypic transformation of VSMCs induced by LPS,and its mechanism may be related to NF-κB signaling pathway.
作者 贾鑫 王锋 刘宝辉 杨凯强 王玉玖 董圣军 JIA Xin;WANG Feng;LIU Baohui;YANG Kaiqiang;WANG Yujiu;DONG Shengjun(Binzhou Medical University Hospital,Binzhou 256600,China)
出处 《药学研究》 CAS 2022年第9期570-573,共4页 Journal of Pharmaceutical Research
基金 山东省医药卫生科技发展计划项目(No.2019WS327) 山东省中医药科技项目(No.2021M166)。
关键词 仙茅苷 血管平滑肌细胞 细胞增殖 细胞迁移 细胞表型转化 Curculigoside Vascular smooth muscle cells Proliferation Migration Phenotypic transformation
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  • 1季春.仙茅多糖COPb-1和COPf-1的分离纯化及结构研究[J].贵州化工,2005,30(1):17-19. 被引量:16
  • 2于存涛,孙立忠,常谦,朱俊明,刘永民.应用四分支血管分段停循环下全胸腹主动脉替换术[J].中华医学杂志,2006,86(3):167-169. 被引量:28
  • 3Ross R. Cell biology of atherosclerosis. Annu Rev Physiol 2001; 57: 791-804.
  • 4Pandian RP, Kutala VK, Liaugminas A, Parinandi NL, Kuppusamy P. Lipopolysaccharide-induced alterations in oxygen consumption and radical generation in endothelial cells. Mol Cell Biochem 2005; 278: 119-27.
  • 5Fasanaro P, Magenta A, Zaccagnini G, Cicchillitti L, Fucile S, Eusebi F, et al. Cyclin DI degradation enhances endothelial cell survival upon oxidative stress. FASEB J 2006; 20: 1242-4.
  • 6Xu HB, Huang ZQ. Icariin enhances endothelial nitric-oxide synthase expression on human endothelial ceils in vitro. Vascul Pharmacol 2007; 47: 18-24.
  • 7Gottfried JL, Michael G, Heidrun L, Brigitte S, Julia K, Sylvia K, et al. Prostaglandin E1 does not influence plasmatic coagulation, hepatic synthesis, or postoperative blood loss in patients after coronary-artery bypass grafting. J Clin Anesth 2000; 12: 363-70.
  • 8Tauber S, Menger M, Lehr H. Microvascular in vivo assessment of reperfusion injury: significance of prostaglandin E1 and 12 in postischemic "No-Reflow" and "Reflow-Paradox'. J Surg Res 2004; 120: 1-11.
  • 9Sinha AK, Colman RW. Prostaglandin E1 inhibits platelet aggregation by a pathway independent of adenosine 3',5'-monophosphate. Science 1978; 200: 202-3.
  • 10Marchesi S, Pasqualini L, Lombardini R, Vaudo G, Lupattelli G, Pirro M, et al. Prostaglandin E1 improves endothelial function in critical limb ischemia. J Cardiovasc Pharmacol 2003; 41: 249-53.

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