EPA、DHA对脂多糖诱导的大鼠系膜细胞增殖及凋亡的影响

山东大学学报(医学版)

EPA、DHA对脂多糖诱导的大鼠系膜细胞增殖及凋亡的影响

耿文静¹,柳方娥¹,焦波²,程艳娜²

山东大学 1. 第二医院儿科; 2. 药学院药理教研室, 济南 250012

收稿日期:2007-08-28 修回日期:1900-01-01 出版日期:2008-01-16 发布日期:2008-01-16
通讯作者: 柳方娥

Effects of EPA and DHA on the proliferation and apoptosis of glomerular mesangial cells induced by lipopolysaccharide

GENG Wen-jing¹,LIU Fang-e¹,JIAO Bo²,CHENG Yan-na²

1. Department of Pediatrics, Second Hospital of Shandong University; 2. Department of Pharmacology, School of Pharmacy, Shandong University, Jinan 250012, China

Received:2007-08-28 Revised:1900-01-01 Online:2008-01-16 Published:2008-01-16
Contact: LIU Fang-e

摘要/Abstract

摘要： 摘要：目的观察二十碳五烯酸(EPA)和二十二碳六烯酸(DHA)对正常及在脂多糖(LPS)诱导下的肾小球系膜细胞(GMCs)增殖和凋亡的影响。方法EPA和DHA各设两个终浓度(10μmol／L和100μmol／L),LPS终浓度为10μg／mL,培养时间为24、48和72h,采用MTT法测定细胞增殖;EPA和DHA终浓度为100μmol／L,培养48h后,采用双染色流式细胞术检测细胞凋亡。结果EPA和DHA对正常GMCs无明显影响;对LPS诱导的GMCs增殖有明显抑制作用(P＜0.01),在同等浓度下,DHA的作用强于EPA(P＜0.01);EPA、DHA可明显促进GMCs凋亡。结论EPA和DHA明显抑制LPS诱导的GMCs增殖并促进其凋亡。

Abstract: To observe the effects of EPA and DHA on the proliferation and apoptosis of glomerular mesangial cells(GMCs) induced by lipopolysaccharide(LPS). MethodsThe GMCs were incubed with EPA and DHA at concentrations of 10μmol／L and 100μmol／L for 24, 48 and 72hs. The proliferation of GMCs was determined by MTT. The apoptosis of GMCs was determined by flow cytometry. ResultsBoth EPA and DHA had no effect on the proliferation of normal GMCs. The proliferation of GMCs induced by LPS was significantly inhibited. DHA was more effective than EPA at the same concentration. The apoptosis of GMCs was promoted by EPA and DHA(100μmol／L). ConclusionEPA and DHA could inhibit the proliferation and promote the apoptosis of GMCs induced by LPS.

Key words: Eicosapentaenoic acid, Docosahexaenoic acid, Mesangical cell, ProliferationIgA

中图分类号:

R692-6

耿文静,柳方娥,焦波,程艳娜 . EPA、DHA对脂多糖诱导的大鼠系膜细胞增殖及凋亡的影响[J]. 山东大学学报(医学版), 2008, 46(1): 37-59.

GENG Wen-jing,LIU Fang-e,JIAO Bo,CHENG Yan-na. Effects of EPA and DHA on the proliferation and apoptosis of glomerular mesangial cells induced by lipopolysaccharide[J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2008, 46(1): 37-59.

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