L-氨基胍对体外培养退变椎间盘细胞中炎性因子水平的影响  被引量:3

Influence of L-aminoguanidine in inflammatory factor levels in degenerate intervertebral disc cells in vitro

在线阅读下载全文

作  者:符俏[1,2] 虞乐华[1] 

机构地区:[1]重庆医科大学附属第二医院康复医学科,重庆404100 [2]海南省人民医院康复医学科,海南海口570311

出  处:《吉林大学学报(医学版)》2014年第1期35-38,共4页Journal of Jilin University:Medicine Edition

基  金:国家自然科学基金资助课题(81171859);重庆市卫生局科研基金资助课题(2010-1-20;2011-2-172)

摘  要:目的:研究一氧化氮合酶(NOS)抑制剂L-氨基胍(L-AG)对体外培养的退变椎间盘细胞中炎性因子水平的影响,并探讨其作用机制。方法:采用体外培养的退变椎间盘细胞为研究对象,根据L-AG浓度分为0(对照组)、0.5%、1.0%和1.5%组,作用24h后,分光光度法检测NOS活性和一氧化氮(NO)水平,免疫印迹法检测炎性因子白细胞介素1(IL-1)、白细胞介素6(IL-6)以及肿瘤坏死因子α(TNF-α)的表达水平。结果:0.5%、1.0%、1.5%L-AG组退变椎间盘细胞中NOS活性分别为6.1、5.5和4.2U·mL-1,NO水平分别为128.3、116.5和97.7μmol·L-1,与对照组比较均显著降低(P<0.01);与对照组比较,不同浓度L-AG组退变椎间盘细胞中IL-1、IL-6及TNF-α表达水平均显著降低(P<0.01)。结论:NOS抑制剂L-AG可显著降低退变椎间盘细胞炎性反应,其作用机制可能与NOS抑制有关。Objective To study the influence of nitric oxide synthase (NOS) inhibitor L-aminoguanidine (L-AG) in the inflammatory factor levels in degenerate intervertebral disc cells in vitro, and to explore its mechanism. Methods After treatment with L-AG (0, 0.5%, 1.0%, 1.5%) for 24 h, the levels of NO and the activities of NOS were detected with spectrophotometric method and the expression levels of IL-1, IL-6 and TNF-α were determined by Western blotting. Results The activities of NOS in degenerate intervertebral disc cells in 0. 5%, 1.0%, 1.5% L-AG groups were 6.1, 5.5, and 4.2 U · mL-1; the NO levels were 128.3, 116.5, and 97.7 μmol · L-1 , respectively, which were significantIy lower than those in OL-AG group (control group) (P〈 0. 05). Compared with control group, the expression levels of IL-1, IL-6 and TNF-α in 0.5%, 1.0%, and 1.5% L-AG groups were also significantly reduced (P〈0. 01-0.05). Oonclusion L-AG can reduce the inflammatory reaction of degenerate intervertebral disc cells, which may be related to inhibition of NOS.

关 键 词:L-氨基胍 退变椎间盘细胞 一氧化氮合酶 炎性因子 

分 类 号:R681.5[医药卫生—骨科学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象