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目的探讨48 h半数致死量(LD50)脂多糖对长期铅暴露小鼠致死率及外周血炎症因子的影响。方法将100只健康初断乳21日龄清洁级雄性昆明小鼠随机分为5组,分别为空白(蒸馏水)组、对照组和低(200 mg/L)、中(400mg/L)、高(800 mg/L)剂量乙酸铅+LPS(LD50,8.6 mg/kg)染毒组,每组20只。采用自由饮水方式进行铅染毒,连续染毒12周;再一次性腹腔注射染毒LPS,染毒容量为2.5 ml/kg,空白组注射等体积的生理盐水。统计48 h的死亡数并计算死亡率;检测外周血白细胞介素6(interleukin-6,IL-6)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、γ-干扰素(interferon-γ,IFN-γ)及高迁移率组蛋白1(high mobility group box 1,HMGB1)的浓度。结果与对照组比较,400、800mg/L乙酸铅+LPS染毒组小鼠48 h死亡率均明显升高,差异有统计学意义(P<0.05);且随着乙酸铅染毒剂量的升高,小鼠48 h死亡率呈上升趋势。与对照组比较,各剂量乙酸铅+LPS染毒组小鼠血清IL-6、TNF-α、IFN-γ水平均下降,而HMGB1水平均升高,差异有统计学意义(P<0.05);且随着乙酸铅染毒剂量的升高,小鼠血清IL-6、TNF-α、IFN-γ水平呈下降趋势,HMGB1水平呈上升趋势。结论长期铅暴露可导致小鼠的抗感染能力下降。
Objective To investigate the effects of 48 h LD50 lipopolysaccharide on lethality and inflammatory cytokines in mice exposed to chronic lead exposure. Methods A total of 100 healthy primary weaned 21-day-old male Kunming mice were randomly divided into 5 groups: blank (distilled water) group, control group and low (200 mg / L) (800 mg / L) dose of lead acetate + LPS (LD50, 8.6 mg / kg). The rats were exposed to lead for 12 weeks. The rats were injected intraperitoneally with LPS for 2.5 ml / kg. The rats in the blank group were injected with the same volume of normal saline. The number of deaths after 48 h was calculated and the mortality was calculated. The levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and interferon-γ interferon-γ, IFN-γ) and high mobility group box 1 (HMGB1). Results Compared with the control group, the 48 h mortality rates in 400, 800 mg / L lead acetate + LPS group were significantly increased (P <0.05), and with the increase of lead acetate dose High, mice 48 h mortality is on the rise. Compared with the control group, the levels of IL - 6, TNF - α and IFN - γ in the serum of the mice treated with lead acetate and LPS decreased, but the levels of HMGB1 increased (P <0.05). The level of IL-6, TNF-α and IFN-γ in serum of mice decreased and the level of HMGB1 increased with the increase of lead acetate dose. Conclusion Long-term lead exposure can lead to a decrease in the anti-infective capacity of mice.