α黑素细胞刺激素保护内毒素休克小鼠的免疫学机制研究  被引量:2

Study on the Immunological Mechanism of Protective Effect of α-Melanocyte Stimulating Hormone on Mice with Endotoxic Shock

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作  者:韩德平[1] 田野苹[1] 张明徽[1] 赵勇[1] 周正芳[1] 郑玲莉[1] 

机构地区:[1]第二军医大学免疫学教研室,上海200433

出  处:《上海免疫学杂志》2001年第2期70-73,共4页Shanghai Journal of Immunology

基  金:全军医药卫生科研基金资助项目! (NO98M0 73 )

摘  要:为研究α黑素细胞刺激素 (α MSH)对内毒素休克小鼠发挥保护作用的免疫学机制 ,将BALB/c小鼠经腹腔注射 (ip)LPS5 0 μg/kg和D 半乳糖胺 (D Gal) 90 0mg/kg建立内毒素休克模型后 ,在不同时间给予α MSHip后观察小鼠的存活率 ;用MTT法测定小鼠血清中IL 1、TNF α、IL 6的含量 ;用Griess试剂测定血清中NO的含量。腹腔巨噬细胞 (MΦ)膜表面免疫相关分子以流式细胞仪检测。结果是给予LPS前 1h、同时和后 1hα MSH 2 5mg/kgip可以明显提高内毒素休克小鼠的存活率 ,其中以给予LPS 1h后注射α MSH疗效最佳 ,能显著降低血清中IL 1、TNF α含量 (P <0 0 0 1) ,增加IL 6的产生 (P <0 0 5 ) ,抑制LPS引起的腹腔MΦ高表达CD14、CD40、CD5 4及CD86分子。因此 ,α MSH降低TNF α、IL 1及NO的含量 ,抑制MΦ膜表面CD14、CD5 4、CD40及CD86的表达 ,在其抗内毒素休克效应中起重要作用。To investigate the immunological mechanism of the protective effect of α melanocyte stimulating hormone(α MSH) in mice with endotoxic shock,experimental model of mouse with endotoxic shock was established by intraperitoneal injections of LPS(50 μg/kg) and D galactosamine(900 mg/kg),and the survival times of mice recieving α MSH at different times were observed with simultaneous determinations of serum contents of IL 1,TNF α,and IL 6 by MTT assay and the serum content of NO as determined by Griess reagent The expression of membrane molecules on the surface of peritoneal macrophages was analyzed by FACS It was found that the survival times of mice with endotoxic shock giving LPS one hour before,simultanously and one hour after were markedly prolonged with the most effective time of administrating α MSH to mice one hour after giving LPS Also,this treatment could significantly decrease the serum contents of IL 1,TNF and NO,but improve the production of IL 6 and inhibit the high expressions of CD14,CD40,CD54 and CD86 molecules on the surface of peritoneal macrophages It suggests that α MSH might be an important factor in the protective effect in mice with endotoxic shock

关 键 词:Α黑素细胞刺激素 内毒素休克 促炎症细胞因子 一氧化氮 巨噬细胞 免疫学 

分 类 号:R631.4[医药卫生—外科学]

 

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