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游离脂肪酸及葡萄糖对鼠主动脉内皮细胞的影响及作用机制
引用本文:郭海莲,刘晓玲,李鹏翠,韩乐,王东青.游离脂肪酸及葡萄糖对鼠主动脉内皮细胞的影响及作用机制[J].中国现代医生,2012,50(10):4-7.
作者姓名:郭海莲  刘晓玲  李鹏翠  韩乐  王东青
作者单位:1. 山西医科大学研究生院,山西太原,030001
2. 山西医科大学第二临床医院干部内分泌科,山西太原,030001
3. 山西医科大学第二临床医院骨科实验室,山西太原,030001
基金项目:山西省留学归国人员科研基金(200372)
摘    要:目的探讨高糖高游离脂肪酸(freefattyacids,FFAs)对内皮细胞增殖和凋亡的影响及其作用机制。方法原代培养大鼠主动脉内皮细胞(rataortaendothelialcell,RAEC),采用不同浓度的葡萄糖(5.5mmol/L,30mmol/L)及棕榈酸(200μmol/L、400μmol/L、600μmol/L)单独或联合作用于细胞24h、48h、72h。免疫组织化学染色方法鉴定内皮细胞并测定IL-8、Bcl-2、BAX表达水平:MTT比色法检测细胞增殖率。结果FFAs及葡萄糖单独及联合应用均可导致细胞出现凋亡形态学变化,增殖呈剂量-时间依赖性(P〈0.05),且联合组明显低于单独培养组(P〈0.01);干预后IL-8、BAX表达增加,Bcl-2蛋白表达逐渐减弱,Bcl-2/BAX比值逐渐减小,联合培养组表达更为明显。结论高浓度FFAs及高糖具有抑制内皮细胞生长、促进其凋亡的作用,其作用机制可能是通过葡萄糖及棕榈酸酯参与P13K/AKT等途径激活氧化应激诱导细胞凋亡。

关 键 词:糖尿病  游离脂肪酸  内皮细胞  bcl-2  BAX  P13K/AKT

Influence and mechanism of free fatty acid and glucose on endothelial cell of rat aorta
Authors:GUO Hailian  LIU Xiaoling  LI Pengcui  HAN Le  WANG Dongqing
Affiliation:1.Graduate School of Shanxi Medical University,Taiyuan 030001,China;2.Department of Endocrinology,the Second Affiliated Hospital of Shanxi Medical University,Taiyuan 030001,China;3.Department of Orthopaedic Laboratory,the Second Affiliated Hospital of Shanxi Medical University,Taiyuan 030001,China
Abstract:Objective To explore the influence and mechanism of free fatty acid(FFAs) and glucose on endothelial cell proliferation and apoptosis.Methods Rat aorta endothelial cell(RAEC)were cultured in vitro,glucose(5.5 mmol/L,30 mmol/L) and palmitic acid(200 μmol/L、400 μmol/L、600 μmol/L) in different concentration were applied,alone and together,to RAEC for 24 h,48 h,72 h.Immunohistochemistry were used to determine CD31-related antigen and detected IL-8,Bcl-2,BAX protein expression changes;Applied four methyl azo thiazole blue(determined by MTT) colorimetric detection different environment RAEC proliferation capacity.Results Glucose and FFAs,alone and together,can lead to apoptotic morphological changes in RAEC;FFAs and glucose display strong growth inhibitory effect in a-time and does-development manner against RAEC(P < 0.05),and the combination group was significantly lower than the proliferation of cultured alone group(P < 0.01).After intervention,IL-8,BAX expression were increased,Bcl-2 protein expression were gradually decreased,Bcl-2/BAX ratio wrere decreased,and more obvirous expression of the combination group.Conclusion High FFAs and high glucose can inhibit the growth of RAEC and promote their apoptosis,its mechanism may be involved by glucose and palmitate PI3K/AKT pathway activation oxidative stress-induced apoptosis.
Keywords:Diabetes mellit  Free fatty acid  Endothelial cell  bcl-2  BAX  PI3K/AKT
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