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大鼠保护性热应激模型中肿瘤坏死因子及一氧化氮的研究
引用本文:王斌,刘瑶,罗炳德.大鼠保护性热应激模型中肿瘤坏死因子及一氧化氮的研究[J].中华劳动卫生职业病杂志,2002,20(1):13-15.
作者姓名:王斌  刘瑶  罗炳德
作者单位:1. 510515,广州,第一军医大学热带军队卫生学系高温医学研究室
2. 510515,广州,第一军医大学附属南方医院惠侨科
基金项目:“九五”军队指令性课题 ( 96L0 33)
摘    要:目的 通过研究保护性热应激模型建立过程中肿瘤坏死因子 (tumornecrosisfactor,TNF)及一氧化氮 (nitricoxide,NO)的动态变化规律及其作用 ,为该模型的建立提供进一步的理论依据。方法 给予大鼠适量热应激处理 ,然后分离血清 ,分别用放射免疫均相竞争法和硝酸还原酶法测定热应激后 0~ 2 4h不同时相TNF、NO的浓度。结果 热应激后 2、4、8、12h ,TNF浓度升高 ,与对照组比较 ,差异有显著性 (P <0 .0 5、P <0 .0 1) ,0h、2 4h与对照组的差异无显著性 (P >0 .0 5 )。热应激后 4h ,血清TNF浓度达到峰值 (3.35± 0 .2 0 )ng/ml],较 0h和 2h明显升高 ,差异有显著性 (P <0 .0 1) ,8、12、2 4h较 4h明显降低 ,差异有显著性 (P <0 .0 5、P <0 .0 1) ,2 4h恢复到正常水平。热应激后 2、4、8、12、2 4h ,大鼠血清NO浓度较对照组升高 ,差异有显著性 (P <0 .0 5 )。热应激后 8h ,NO浓度达到峰值 (10 8.2 1± 2 7.89) μmol/L],与 0、2、4h比较 ,差异有显著性 (P <0 .0 1) ,12h开始下降 ,与 8h比 ,差异有显著性 (P <0 .0 5 ) ,2 4h进一步降低 ,但仍然高于对照组。结论 保护性热应激模型建立过程中TNF、NO起了很重要的作用。

关 键 词:保护性热应激模型  肿瘤坏死因子  一氧化氮  热休克蛋白  大鼠
修稿时间:2001年3月20日

Tumor necrosis factor and nitric oxide in the protective heat stress model
WANG Bin,LIU Yao,LUO Bingde.Tumor necrosis factor and nitric oxide in the protective heat stress model[J].Chinese Journal of Industrial Hygiene and Occupational Diseases,2002,20(1):13-15.
Authors:WANG Bin  LIU Yao  LUO Bingde
Institution:Department of Tropical Military Hygiene, First Military Medical University, Guangzhou 510515, China.
Abstract:OBJECTIVE: To investigate the variation and the effect of TNF and NO in the process of the creation of protective heat stress model and provide more thoretical basis. METHODS: The rats were properly treated with heat and then the serum was separated. Radioimmunoassay and nitrate reductase assay were employed to measure the concentration of TNF and NO at different time between 0 h and 24 h after heat stress respectively. RESULTS: Compared with the control, the concentration of TNF increased significantly 2 h, 4 h, 8 h, 12 h after heat stress, of which 2 h, 12 h(P < 0.05), 4 h, 8 h(P < 0.01), but no significant changes 0 h, 24 h after heat stress. The concentration reached the peak 4 h after heat stress(3.35 +/- 0.20) ng/ml] and increased significantly than 0 h, 2 h, 8 h, 12 h, 24 h after heat stress(P < 0.01, P < 0.05). 24 h after heat stress it recovered to normal standard. Compared with the control, the concentration of NO was higher 2 h, 4 h, 8 h, 12 h, 24 h after heat stress(P < 0.05), but no significance at 0 h. The concentration amounted to peak 8 h after heat stress(108.21 +/- 27.89) mumol/L] and increased than 0 h, 2 h, 4 h after heat stress(P < 0.01). After 8 h it began to decrease continuously in heat stress group, however it was higher 24 h after heat stress than control. CONCLUSION: TNF and NO played an important role in the process of the creation of protective heat stress model.
Keywords:Heat stress model  Tumor necrosis factor  Nitric oxide  Heat shock protein
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