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端礼荣, 张志坚, 陆荣柱, 卢隽滢, 陈燕, 陆子阳. 氯化锂致小鼠腹腔巨噬细胞功能抑制作用[J]. 中国公共卫生, 2010, 26(1): 93-94. DOI: 10.11847/zgggws2010-26-01-50
引用本文: 端礼荣, 张志坚, 陆荣柱, 卢隽滢, 陈燕, 陆子阳. 氯化锂致小鼠腹腔巨噬细胞功能抑制作用[J]. 中国公共卫生, 2010, 26(1): 93-94. DOI: 10.11847/zgggws2010-26-01-50
DUAN Li-rong, ZHANG Zhi-jian, LU Rong-zhu, . Inhibitory effect of lithium chioride on function of peritoneal macrophage in mice[J]. Chinese Journal of Public Health, 2010, 26(1): 93-94. DOI: 10.11847/zgggws2010-26-01-50
Citation: DUAN Li-rong, ZHANG Zhi-jian, LU Rong-zhu, . Inhibitory effect of lithium chioride on function of peritoneal macrophage in mice[J]. Chinese Journal of Public Health, 2010, 26(1): 93-94. DOI: 10.11847/zgggws2010-26-01-50

氯化锂致小鼠腹腔巨噬细胞功能抑制作用

Inhibitory effect of lithium chioride on function of peritoneal macrophage in mice

  • 摘要: 目的 观察氯化锂(LiCl)对巨噬细胞功能抑制作用。方法 以0.4,0.6,1.2mg/(kg·bw)LiCl连续给小鼠灌胃20d后进行巨噬细胞吞噬功能、产生NO能力及产生H2O2等指标的检测。结果 各LiCl剂量组小鼠腹腔灌洗液细胞数减少,与对照组比较差异有统计学意义;巨噬细胞吞噬功能受到明显抑制,抑制率分别为27.7%,40.2%,43.8%,且呈现剂量-反应关系(P<0.05);巨噬细胞产生NO的能力也受到明显抑制,对照组为(54.21±12.55)μmol/L,其余各组分别为(42.36±14.22),(25.64±12.42),(37.82±13.48)μmol/L;巨噬细胞产生的O-2在3种剂量下均出现明显抑制,呈现剂量-反应关系(P<0.05),巨噬细胞产生H2O2的能力仅在1.2mg/kg剂量时出现明显抑制,与对照组比较差异有统计学意义,但H2O2的产生与LiCl剂量亦存在剂量-反应关系。结论 LiCl在0.4,0.6,1.2mg/(kg·bw)剂量下对巨噬细胞吞噬功能,NO、O-2、H2O2等生物分子的产生均有明显抑制作用,与LiCl可直接影响巨噬细胞的抗原递呈及非特异性防御功能有关。

     

    Abstract: Objective To observe the inhibitory effect of lithium chloride(LiCl)on macrophage function.Methods Phagocytic function,abilities to produce nitrous oxide and hydrogen peroxide of macrophage in mice were dete rmined 20 days after they were admin istered continuously with LiCl at the doses of 0.4,0.6,and 1.2 mg/kg·bw.Results Compared with the control group,phagocytic function of macrophage of LCil treated mice was inhibited significantly with inhibition rates of 27.7%,40.2%,and 43.8%,respectively in a dose-response pattern.The ability of microphage to produce nitrous oxide was significantly inhibited also(42.36±14.22,25.64±12.42,37.82±13.48 μmol/L for the LiCl dose of 0.4,0.6,1.2 mg/kg·bw,respectively)compared with 54.21?12.55 μmol/L of the control group.The ability of microphage to produce O-2 was obvio usly inhibited by LiCl in a dose-response manner(P<0.05).The ability of microphage to produce hydrogen peroxide was inhibited only at a dose of 1.2 mg/kg·bw of LiCl with a significant difference compared with the control guoup.Conclusion At doses of 0.4,0.6,and 1.2 mg/kg·bw,LiCl couldinhib it the phago cytic fumction of microphage and the production of biologicalm olecules such as nitrous oxide,O-2,and hydrogen peroxide.

     

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