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EGCG对高糖培养的系膜细胞增殖及周期素激酶抑制剂P27的作用 被引量:2

Effect of EGCG on Mesangial Cells Proliferation Cultured Condition and Expression of Cyclin Kinase Inhibitor p27 in High Glucose
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摘要 目的:探讨表没食子儿茶素没食子酸脂(EGCG)对高糖培养的系膜细胞(GMCs)增殖及周期素激酶抑制剂p27蛋白表达的作用。方法:以大鼠肾系膜细胞为实验对象,将GMCs分成6组,分别刺激48h后,用四甲基偶氮唑蓝(MTT)测定GMCs增殖情况,Westernblot法测定p27蛋白表达。结果:作用48h后,高糖明显诱导GMCs增殖并上调p27蛋白表达,不同浓度的EGCG能抑制高糖诱导的细胞增生,并抑制p27蛋白表达。结论:EGCG能抑制高糖诱导的GMCs增殖,并下调p27蛋白表达,提示EGCG可通过抑制p27表达而减少细胞外基质的积聚,延缓糖尿病肾小球肥大和肾小球硬化。 The effect of epigallocatechin-3-gallate (EGCG) on rat inesangial cells (GMCs) proliferation cultured in high glucose condition and the expression of cyclin kinase inhibitor p27(p27) protein were investigated. The GMCs were divided into 6 groups. 48 hours later, the proliferation activity of GMCs was observed by MTT assay, the expression of p27 protein was enhanced by Western blot. Results showed that compared with normal glucose group, high glucose treatment significantly increased GMCs proliferation activity and the expression of p27 protein. EGCG in different concentration suppressed the proliferation of GMCs and down-regulated the expression of p27. It can be concluded that EGCG can suppress the proliferation activity of GMCs cultured under high glucose and decrease the expression of p27 protein, which implied EGCG probably decrease the accumulation of extracellular matrix (ECM) and slowed the progession of progression of glomerular hypertrophy and glomerulosclerosis in diabetic nephropathy.
出处 《茶叶科学》 CAS CSCD 北大核心 2005年第4期307-310,共4页 Journal of Tea Science
关键词 EGCG 周期素激酶抑制剂 系膜细胞 糖尿病肾病 EGCG, Mesangial cell, Diabetic nephropathy, Cyclin kinase inhibitor p27
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参考文献5

  • 1Awazu M, Omori S, Ishikura K, et al. The lack of cyclin kinase inhibitor p27(Kipl) ameliorates progression of diabetic nephropathy[J]. J Am Soc Nephrol. 2003, 14(3):699~708.
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同被引文献14

  • 1李彩蓉,蔡飞,杨晓,朱忠华.EGCG对糖尿病大鼠肾氧化应激的影响[J].咸宁学院学报(医学版),2005,19(4):283-286. 被引量:8
  • 2杨晓,李彩蓉,蔡飞,朱忠华,卢远航.表没食子儿茶素没食子酸酯对糖尿病大鼠肾脏细胞外调节蛋白激酶活性的影响[J].中华肾脏病杂志,2007,23(3):184-188. 被引量:3
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  • 5Li J J, Kwak SJ, Jung DS, et al. Podocyte biology in diabetic nephropathy. Kidney Int, 2007,106(Suppl) : S36 - S42.
  • 6Shankland SJ, Hugo C, Coats SR, et al. Changes in cell cycle protein expression during experimental mesangial proliferative glomerulonephritis. Kidney Int, 1996,50(4) : 1230 - 1239.
  • 7Mundel P, Shankland SJ. Podocyte biology and response to injury.J Am Soc Nephrol,2002,13(12):3005 -3015.
  • 8Kim YG, Alpers CE, Brugarolas J, et al. The cyclin kinase inhibitor p21^Cip1/waf1 limits glomerular epithelial cell proliferation in experimental glomerulonephritis. Kidney Int, 1999, 55 (6) :2349 - 2361.
  • 9Kanwar YS,Akagi S, Sun L, et al. Cell biology of diabetic kidney disease. Nephron Exp Nephrol, 2005,101 (4) :e100 - e110.
  • 10Ahmad N, Cheng D, Mukhtar H. Cell cycle dysregulation by green tea polyphenol epigallocatechin- 3 - gallate. Biochem Biophys Res Commun, 2000,275 (2) : 328 - 334.

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