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[1]吴勇,叶芬,葛轶睿,等.SN50对缺血再灌注损伤中TNF-α影响的实验研究[J].医学研究与战创伤救治(原医学研究生学报),2014,16(05):453-455.[doi:10.3969/j.issn.1672-271X.2014.05.002]
　WU Yong,YE Fen,GE Yi-rui,et al.Experimental study of SN50 on TNF-α effects in ischemia-reperfusion injury[J].JOURNAL OF MEDICALRESEARCH —COMBAT TRAUMA CARE,2014,16(05):453-455.[doi:10.3969/j.issn.1672-271X.2014.05.002]
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SN50对缺血再灌注损伤中TNF-α影响的实验研究()
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《医学研究与战创伤救治》（原医学研究生学报）[ISSN:1672-271X/CN:32-1713/R]

卷:
第16卷
期数:
2014年05期
页码:
453-455
栏目:
出版日期:
2014-09-20

文章信息/Info

Title:
Experimental study of SN50 on TNF-α effects in ischemia-reperfusion injury
作者:
吴勇1; 叶芬1; 葛轶睿1; 陆燕1; 魏锐利2
1.210002 江苏南京，第二军医大学南京临床医学院(南京军区南京总医院)眼科;2.200003上海，第二军医大学附属长征医院眼科
Author(s):
WU Yong1; YE Fen1; GE Yi-rui1; LU Yan1; WEI Rui-li2.
1.Department of Ophthalmology，Nanjing School of Clinical Medicine,Second Military Medical University/Nanjing General Hospital of Nanjing Military Command,PLA,Nanjing,Jiangsu 210002,China;2.Department of Ophthalmology，Changzheng Hospital,Second Military Medical University,Shanghai 200003,China
关键词:
SN50; 巨噬细胞; 肿瘤坏死因子-α; 核转录因子-κB; 缺血再灌注
Keywords:
SN50;  macrophages;  TNF-α;  NF-κB;  ischemia-reperfusion
分类号:
R363
DOI:
10.3969/j.issn.1672-271X.2014.05.002
文献标志码:
A
摘要:
目的研究核转录因子-κB(nuclear factor-kappaB，NF-κB)抑制剂SN50 对氧糖剥夺条件下培养的SD大鼠巨噬细胞炎性因子肿瘤坏死因子-α(tumor necrosis factor-α，TNF-α)表达的影响。方法用MTT法检测SN50对细胞增殖活性的影响，以ELISA 法检测氧糖剥夺条件下SN50对TNF-α表达影响。结果 经SN50处理的氧糖剥夺条件下的巨噬细胞成活率较未经处理的明显上升(P<0.05或P<0.01)，TNF-α表达的上调幅度亦明显变小(P<0.05或P<0.01)。结论SN50主要是通过抑制NF-κB 核的移位干扰了TNF-α 的基因转录而导致其合成的蛋白量降低。
Abstract:
Objective To study the effect of SN50,the nuclear factor kappa B (NF-κB) inhibitor on the expression of macrophage inflammatory factor TNF-α in the oxygen and glucose deprivation in SD rats.Methods The effect of SN50 on cell proliferation activity was observed by MTT method.The expression of TNF-α in macrophages after treated with SN50 was observed by ELISA.Results The macrophage survival rate was significantly increased after treated with SN50 (P<0.05 or P<0.01).The increase of TNF-α was significantly smaller after treated with SN50 in oxygen glucose deprivation conditions (P<0.05 or P<0.01).Conclusion SN50 reduces the expression of TNF-α in macrophages,mainly through inhibiting the translocation of NF-κB nuclear,which provides a theoretical basis for the clinical treatment of ischemic reperfusion injury.

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备注/Memo

备注/Memo:
国家自然科学基金(81200719)
更新日期/Last Update: 2014-09-20