姜黄素对溶血磷脂酰胆碱诱导内皮细胞炎症因子产生的影响

摘要/Abstract

摘要： 目的: 观察姜黄素对溶血磷脂酰胆碱(LPC) 诱导内皮细胞炎症因子产生的影响, 探讨姜黄素抗动脉粥样硬化(AS) 的作用机制。方法: 体外培养的人脐静脉内皮细胞(HUVECs), 待细胞生长到融合状态时加入不同浓度(25 、50 、100 mg/L) 的姜黄素预处理30 min, 然后加入LPC(5 mg/L) 作用24 h, 用酶联免疫吸附法(ELISA) 检测上清液中细胞间黏附分子-1(ICAM-1) 、单核细胞趋化蛋白-1(MCP-1) 、IL-6 和TNF-α的含量;实时荧光定量PCR (real-time PCR) 检测ICAM-1 、MCP-1 、IL-6 和TNF-αmRNA 的表达;蛋白印迹法(Western blot) 和免疫细胞化学染色法检测核因子-κBp65(NF-κBp65) 蛋白的表达。结果: LPC 能明显增加HUVECs ICAM-1 、MCP-1 、IL-6 、TNF-αmRNA和NF-κBp65 蛋白的表达以及上清液中ICAM-1 、MCP-1 、IL-6 、TNF-α的含量, 而预先应用不同浓度的姜黄素干预后, 上述效应明显减弱, 并且具有剂量依赖性。结论: 姜黄素抑制炎症因子的产生可能与其抑制NF-κB 的活性有关。

关键词: 姜黄素, 溶血磷脂酰胆碱, 内皮细胞, 动脉粥样硬化, 炎症因子

Abstract: AIM: To observe the effects of curcumine on the production of inflammatory factors induced by lysophosphatidylcholine (LPC) and investigate the anti-atherosclerosis mechanism of curcumine.METHODS: The human umbilical vein endothelial cells (HUVECs) were treated with LPC (5 mg/L) for 24 h following pretreatment with various concentrations of curcumine(25, 50, 100 mg/L) for 30 min.Intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1), IL-6 and TNF-αwere determinded by enzyme-linked immunosorbent assay (ELISA) and real-time quantitative reverse transcription-polymerase chain reaction (real-time RT-PCR),the protein expression of nuclearfactor kappa Bp65 (NF-κBp65) was assayed by western blot analysis and immunohistochemical method.RESULTS: The levels and mRNA expression of ICAM-1, MCP-1, IL-6 and TNF-α, and the NF-κBp65 activity were significantly increased by LPC.The increased production of inflammatory factors and NF-κBp65 activity were markedly inhibited by different concentrations of curcumine in a dose-dependent manner.CONCLUSION: Curcumine inhibited the production of inflammatory factors might be related with depressing the activation of NF-κB.

Key words: curcumine, lysophosphatidylcholine, endothelial cells, atherosclerosis, inflammatory factor

中图分类号:

R965.2

李伟军, 刘侨侨. 姜黄素对溶血磷脂酰胆碱诱导内皮细胞炎症因子产生的影响[J]. 中国临床药理学与治疗学, 2009, 14(1): 52-56.

LI Wei-jun, LIU Qiao-qiao. Effects of curcumine on production of inflammatory factors induced by lysophosphatidyl choline in human umbilical vein endothelial cells[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2009, 14(1): 52-56.

参考文献

[1] Barish GD, Atkins AR, Downes M, et al. PPARdelta regulates multiple proinflammatory pathways to suppress atherosclerosis[J]. Pro Natl Acad Sci U S A, 2008, 105(11):4271-4276.
[2] Kaperonis EA, Liapis CD, Kakisis JD, et al. Inflammatory and atherosclerosis[J]. Eur J Vasc Endovasc Surg,2006, 31(4):386-393.
[3] Stool G, Bendszus M.Inflammation and atherosclerosis: novel insights into plaque formation and destabilization[J]. Stroke, 2006, 37(7):1923-1932.
[4] Raza H, John A, Brown EM, et al. Alterations in mitochondrial respiratory functions, redox metabolism and apoptosis by oxidant 4-hydroxynonenal and antioxidants curcumin and melatonin in PC12 cells[J]. Toxicol Appl Pharmacol, 2008, 226(2):161-168.
[5] Chen HW, Lee JY, Huang JY, et al. Curcumin inhibits lung cancer cell invasion and metastasis through the tumor suppressor HLJ1[J]. Cancer Res, 2008, 68(18):7428-7438.
[6] Sandur SK, Pandey MK, Sung B, et al. Curcumin, demethoxycurcumin, bisdemethoxycurcumin, tetrahydrocurcumin and turmerones differentially regulate anti-inflammatory and anti-proliferative responses through a ROS-independent mechanism[J]. Carcinogenesis, 2007, 28(8):1765-1773.
[7] Falk E.Pathogenesis of Atherosclerosis[J]. J Am Col Cardiol, 2006, 47(8 Suppl):C7-12.
[8] Barzilaym JL, Freedland ES.Inflammation and its relationship to insulin resistance, tyke 2 diabetes mellitus, and endothelial dysfunction[J]. Metab Syndr Relat Disord, 2003, 1(1):435-441.
[9] Yang PY, Rui YC, Lu L, et al. Time courses of vascular endothelial growth factor and intercellular adhesion molecule-1 expressions in aortas of atherosclerotic rats[J]. Life Sci, 2005, 77(20):2529-2539.
[10] Kang DG, Moon MK, Lee AS, et al. Cornuside suppressed cytokine-induced pro-inflammatory and adhesion molecules in the human umbilical vein endothelial cells[J]. Biol Pharm Bull, 2007, 30(9):1796-1799.
[11] Naya M, Tsukamoto T, Morita K, et al. Plasma interleukin-6 and tumor necrosis factior-alpha can predict coronary endothelial dysfunction in hypertensive patients[J]. Hypertens Res, 2007, 30(6):541-548.
[12] Ridker PM, Rifain N, Stampfer MJ, et al. Plasma concentration of interleukin 6 and the risk of future myocardial infarction among apparently healthy men[J]. Circulation, 2000, 101(15):1767-1772.
[13] Adibhatla RM, Dempsy R, Hatcher JF.Integration of cytokine biology and lipid metabolism in stroke[J]. Front Biosci, 2008, 13:1250-1270.

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