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。
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 determined 20 days after they were administered 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 LiCl 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 LiCI 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 obviously inhibited by LiCI 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 could inhibit the phagocytic fumction of rnicrophage and the production of biological molecules such as nitrous oxide ,O-2 ,and hydrogen peroxide.
出处
《中国公共卫生》
CAS
CSCD
北大核心
2010年第1期93-94,共2页
Chinese Journal of Public Health
基金
江苏省教育厅自然科学基金资助项目(02KZ030004)
关键词
氯化锂
动物模型
巨噬细胞
吞噬功能
体外培养
lithium chloride
animal model
microphage
phagocytosis
culture in vitro