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目的观察亚砷酸钠对雄性大鼠的肺损伤作用,探讨其细胞衰老作用机制。方法无特定病原体级健康成年雄性Wistar大鼠随机分为对照组和低、中、高剂量组,每组8只,对照组大鼠予饮用超纯水,3个剂量组大鼠予饮用质量浓度分别为10、100和1 000μg/L的亚砷酸钠溶液,连续染毒4周后处死,进行肺组织病理学检查,并采用酶联免疫吸附实验测定大鼠支气管肺泡灌洗液(BALF)中白细胞介素(IL)-1β、IL-6、IL-10有β-半乳糖苷酶(β-Gal)水平。结果低、中和高剂量组大鼠肺组织均出现肺损伤的早期炎症性病理改变;随着染毒剂量的增加,逐渐出现肺泡间隔增宽、蛋白性水肿液渗出和大量炎症细胞浸润等改变。中和高剂量组大鼠BALF中IL-1β、IL-6和β-Gal水平均高于对照组(P<0.05),低、中和高剂量组大鼠BALF中IL-10水平均低于对照组(P<0.05)。大鼠BALF中β-Gal水平和IL-1β、IL-6水平均呈正相关[相关系数(r)分别为0.691和0.410,P<0.05)];β-Gal水平和IL-10水平不相关(r=-0.117,P>0.05)。结论亚砷酸钠经饮水染毒可导致雄性大鼠发生炎症性肺损伤,其机制可能与细胞衰老激活炎症网络有关。
Objective To observe the effect of sodium arsenite on lung injury in male rats and explore the mechanism of cell senescence. Methods Healthy adult male Wistar rats without specific pathogen were randomly divided into control group and low, medium and high dose groups, with 8 rats in each group. The rats in control group were given drinking ultrapure water, 10, 100 and 1 000 μg / L sodium arsenite solution respectively. The rats were sacrificed after 4 weeks of continuous exposure for lung histopathology, and bronchoalveolar lavage fluid (BALF) was measured by enzyme linked immunosorbent assay (ELISA) Interleukin (IL) -1β, IL-6, IL-10 has β-galactosidase (β-Gal) levels. Results In the low, middle and high dose groups, the early inflammatory pathological changes appeared in the lung tissue of rats with lung injury. With the increase of exposure dose, alveolar septa broadening, exudation of protein edema and infiltration of inflammatory cells were gradually appeared change. The levels of IL-1β, IL-6 and β-Gal in BALF were significantly higher in middle and high dose groups than those in control group (P <0.05). The levels of IL-10 in BALF were lower in low, middle and high dose groups Control group (P <0.05). The level of β-Gal in BALF of rats was positively correlated with the levels of IL-1β and IL-6 (r = 0.691 and 0.410 respectively, P <0.05); the level of β-Gal was not correlated with IL-10 r = -0.117, P> 0.05). Conclusion Sodium arsenite can cause inflammatory lung injury in male rats by drinking water, and its mechanism may be related to cellular senescence-activated inflammation network.