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C肽对人脐静脉内皮细胞凋亡的影响及其与内皮型一氧化氮合酶表达的相关性分析 被引量:1

Effects of C-peptide on apoptosis induced by hyperglycemia and the relationship between the apoptosis and the expression of eNOS in human umbilical vein endothelial cell (HUVEC)
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摘要 目的探讨C肽对高糖状态下人脐静脉内皮细胞(HUVEC)凋亡的影响,并对凋亡与内皮型一氧化氮合酶(eNOS)表达进行相关性分析。方法内皮细胞凋亡定性用磷脂酰丝氨酸外翻分析(AnnexinV法),凋亡定量采用细胞DNA片段酶联免疫吸附测定法(ELISA)。检测内皮细胞eNOS表达采用半定量逆转录聚合酶链反应(SQRTPCR)法。结果高浓度葡萄糖(33.3mmol/L)使HUVEC凋亡增加(P<0.01),eNOS表达减少,加入生理浓度(1.0nmol/L)或高浓度(50.0nmol/L)C肽后,凋亡显著减少(P<0.05),eNOS表达增加,HUVEC凋亡与eNOS表达相关(r=-0.845,P<0.01)。结论高糖可导致HUVEC凋亡增加;高浓度或生理浓度的C肽可抑制高糖引起的HUVEC凋亡;HUVEC凋亡与eNOS表达呈负相关。 To investigate the effects of C-peptide on apoptosis induced by high glucose and analyze the relationship between the apoptosis and expression of eNOS in HUVEC. Methods We determined the HUVEC apoptosis by Annexin-V, the expression of eNOS mRNA of HUVEC by RT-PCR, the apoptotic quantity of HUVEC by DNA fragment ELISA. Results High level of glucose could increase HUVEC apoptosis (P< 0.01) and reduce the expression of eNOS. After adding physiological or high concentration of C-peptide, the apoptosis decreased and the expressions of eNOS increased markedly, with the relationship coefficient of -0. 854 (P<0.01). Condusion High glucose may induce apoptosis. Physiological or high concentration of C-peptide may reduce the apoptosis induced by hyperglycemia, the relationship between apoptosis and eNOS is negative.
作者 孟东 于德民
出处 《中华糖尿病杂志(1006-6187)》 CSCD 北大核心 2005年第4期293-295,共3页
关键词 C肽 脐静脉 内皮细胞 细胞凋亡 内皮型一氧化氮合酶 基因表达 C-peptide Umbilical vein Endothelum vascular Apoptosis Nitric-oxide synthase
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参考文献9

  • 1黄雌友,文格波,曹仁贤,刘江华,欧阳贵.葡萄糖诱导人血管内皮细胞凋亡及其对bax和bcl-2表达的影响[J].中国糖尿病杂志,2003,11(1):37-41. 被引量:21
  • 2满国彤,凤志慧,张同琳,周孝思.人、猪、鼠血管内皮及平滑肌细胞培养与纯化方法的改进[J].中国组织化学与细胞化学杂志,2001,10(2):128-133. 被引量:21
  • 3Calles-Escandon J, Cipolla M. Diabetes and endothelial dysfunction: a clinical perspective. Endocr Rev,2001,22:36-52.
  • 4Tedgui A, Mallat Z. Apoptosis as a determinant of atherothrombosis. Thromb Haemost,2001,86:420-426.
  • 5Guevara NV,Chen KH,Chan L,et al. Apoptosis in atherosclerosis: pathological and pharmacological implications. Pharmacol Res,2001,44:59-71.
  • 6Choy JC, Granville DJ, Hunt DW, et al. Endothelial Cell Apoptosis: Biochemical Characteristics and Potential Implications for Atherosclerosis. J Mol Cell Cardiol,2001,33:1673-1690.
  • 7Tzeng E, Kim YM,Pitt BR,et al. Adenviral transfer of the inducible nitric oxide synthase gene block endothelial cell apoptosis. Surgery,1997,122: 255-263.
  • 8Hink U, Li H, Mollnau H, et al. Mechanisms underlying endothelial dysfunction in diabetes mellitus. Circ Res,2001,88: e14-e22.
  • 9Kitamura T, Kimura K, Jung BD, et al. Proinsulin C-peptide rapidly stimulates mitogen-activated protein kinases in Swiss 3T3 fibroblasts: requirement of protein kinase C, phosphoinositide 3-kinase and pertussis toxin-sensitive G-protein. Biochem J,2001,355:123-129.

二级参考文献17

  • 1陈孟勤,曹济民.血管活动的个性化[J].生理科学进展,1996,27(3):203-209. 被引量:4
  • 2Baumgartner-Parzer SM, Wagner L, Pettermann M, et al.High-glucose-triggered apoptosis in cultured endothelial cells.Diabetes, 1995,44 : 1323-1327.
  • 3Du XL, Sui GZ, Stockklauser-Farber K, et al. Induction of apoptosis by high proinsulin and glucose in cultured human umbilical vein endothelial cells is mediated by reactive oxygen species. Diabetologia, 1998,41 : 249-256.
  • 4Jaffe EA, Nachman RL, Becker CG, et al. Culture of human endothelial cells derived from umbilical veins: identification by morphologic and immunologic criteria. J Clin Invest, 1973,52 :2745-2756.
  • 5Mizutani M, Kern TS, Lorenzi M. Accelerated death of retinal microvascular cells in human and experimental diabetic retinopathy. J Clin Invest, 1996,97 : 2883-2890.
  • 6Wang JH, Redmond HP, Waston RWG, et al. Induction of human endothelial cell apoptosis requires both beat shock and oxidative stress responses. Am J Physiol, 1997,272 (cell physiol 41) :C1543-1551.
  • 7Bombeli T, Karsan A, Tait JF, et al. Apoptotic Vascular endothelial cells become procoagulant. Blood, 1997, 29: 2429-2442.
  • 8De Bono DP, Yang WD. Exposure to low concentrations of hydrogen peroxide causes delayed endothelial cell death and inhibits proliferation of surviving cell. Atherosclerosis, 1995,114:235-245.
  • 9Steller H. Mechanisms and genes of cellular suicide. Science,1995,267 : 1445-1449.
  • 10Hockenkery DM, Oltval ZN, Yin XM, et al. Bcl-2 functions in an antioxidant pathway to prevent apoptosis. Cell, 1993, 75:241-251.

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  • 1Hansson GK.Inflammation,atherosclerosis and coronary artery disease[J].N Engl J Med,2005,352(16):1685-1695.
  • 2Van Gaal LF,Mertens IL,De Block CE.Mechanisms linking obesity with cardiovascular disease[J].Nature,2006,444(7121):875-880.
  • 3Wu KK,Huan Y.Diabetic atherosclerosis mouse models[J].Atherosclerosis,2007,191(2):241-249.
  • 4Hoffmann A,Baltimore D.Circuitry of nuclear factor kappa B signaling[J].Immunol Rev,2006,210:171-186.
  • 5Chandra D,Ramana KV,Friedrich B,et al.Role of aldose reductase in TNF-alpha-induced apoptosis of vascular endothelial cells[J].Chem Biol Interact,2003,143-144:605-612.
  • 6Shoji T,Koyama H,Morioka T,et al.Receptor for advanced glycation end products is involved in impaired angiogenic response in diabetes[J].Diabetes,2006,55(8):2245-2255.
  • 7Brownlee M.The pathobiology of diabetic complications:a unifying mechanism[J].Diabetes,2005,54(6):1615-1625.
  • 8Brownlee M.Biochemistry and molecular cell biology of diabetic complications[J].Nature,2001,414(6865):813-820.
  • 9Du X,Matsumura T,Edelstein D,et al.Inhibition of GAPDH activity by poly (ADP-ribose) polymerase activates three major pathways of hyperglycemic damage in endothelial cells[J].J Clin Invest,2003,112(7):1049-1057.
  • 10Lu L,Pu LJ,Xu XW,et al.Association of serum levels of glycated albumin,C-reactive protein and tumor necrosis factor-alpha with the severity of coronary artery disease and renal impairment in patients with type 2 diabetes mellitus[J].Clin Biochem,2007,40(11):810-816.

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