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粒细胞集落刺激因子对小鼠急性肝衰竭的保护作用
引用本文:徐旭雯,谭德明,鲁猛厚. 粒细胞集落刺激因子对小鼠急性肝衰竭的保护作用[J]. 中南大学学报(医学版), 2006, 31(4): 543-547
作者姓名:徐旭雯  谭德明  鲁猛厚
作者单位:中南大学湘雅医院传染病研究所,长沙,410008;中南大学湘雅医院传染病研究所,长沙,410008;中南大学湘雅医院传染病研究所,长沙,410008
摘    要:目的:观察重组人粒细胞集落刺激因子(recombinant human granulocyte colony stimulating factor;rhG-CSF)对D-氨基半乳糖(D-galactosamine,D-GaIN)加脂多糖(lipopolysaccharide,LPS)联合诱导的小鼠急性肝衰竭的保护作用,并探讨其机制。方法:D-GAIN/LPS腹腔联合注射制造小鼠急性肝衰竭模型,治疗组小鼠于造模前4h,2h及造模同时予以G-CSF300μg/kg腹腔注射,观察小鼠24h存活率。造模后6h每组随机选择5只小鼠处死,观察肝组织损伤情况,用半定量逆转录一聚合酶链反应和TanonGis3、73软件分析各组小鼠肝组织中肿瘤坏死因子-α(TNF-α)、干扰素-γ(IFN-γ)、白介素-6(IL-6)和白介素-10(IL-10)的表达情况。结果:治疗组小鼠24h存活率明显高于对照组(P〈0.01),造模后6h治疗组小鼠肝组织损伤明显减轻(P〈0.05),肝组织中7YvF-α和IFN-γ的mRNA表达水平明显低于对照组(P〈0.01),IL-6和IL-10的mRNA表达水平明显高于对照组(P〈0.01)。结论:G-CSF对D-GalN/LPS所致的小鼠急性肝衰竭具有保护作用。

关 键 词:急性肝衰竭  粒胞集落刺激因子  脂多糖  细胞因子
文章编号:1672-7347(2006)04-0543-05
收稿时间:2005-08-29
修稿时间:2005-08-29

XU Xu-wen,TAN De-ming,LU Meng-hou.
Authors:XU Xu-wen  TAN De-ming  LU Meng-hou
Affiliation:Institute of Infectious Diseases, Xiangya Hospital, Central South University, Changsha 410008, China.
Abstract:OBJECTIVE: To evaluate the protective effect of recombinant human granulocyte colony stimulating factor (rhG-CSF) on acute hepatic failure induced by galactosamine (D-GalN) and lipopolysaccharide (LPS) in mice, and to explore its mechanism. METHODS: The mice were intraperitoneally administered D-GalN (800 mg/kg) and LPS (10 microg/kg), and then were intraperitoneally injected either saline (the control group )or rhG-CSF at 300 microg/kg body weight (the therapy group) at 4 h, 2 h and 0 h before the D-GalN/LPS injection. The survival rate of the mice was estimated at 24 h after the D-GalN/LPS injection. The degree of hepatic injury was evaluated at 6 h after the D-GalN/LPS injection, and the levels of TNF-alpha, IFN-gamma, IL-6 and IL-10 mRNA were simultaneously measured by semiquantitative RT-PCR. RESULTS: The survival rate of the therapy group was significantly higher than that of the control group (68.4% vs 20%, P<0.01). As compared with the control group, the degree of liver injury in the therapy group significantly decreased (P<0.05), and the levels of TNF-alpha and IFN-gamma mRNA in the hepatic tissue also reduced remarkably (P<0.01, respectively), while the levels of IL-6 and IL-10 mRNA increased (P<0.01, respectively) at 6 h after the D-GalN/LPS injection. CONCLUSION: G-CSF can protect the mice from acute hepatic failure induced by D-GalN/LPS.
Keywords:acute hepatic failure   granulocyte colony-stimulating factor   lipopolysaccharide    cytokine
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