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目的探讨硒对氟中毒致大鼠肝脏损伤的干预作用。方法以不同方式(先分别喂饲0.375、0.75和1.5mg/L亚硒酸钠溶液6个月,再喂饲50mg/L氟化钠溶液6个月或先饲喂50mg/L氟化钠溶液6个月,再分别饲喂0.375、0.75和1.5mg/L亚硒酸钠溶液6个月)喂饲大鼠,对大鼠肝脏进行组织病理学观察,并测定肝组织谷胱甘肽过氧化物酶(GSH-Px)及超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量及核转录因子κB(NF-κB)表达水平。结果 (1)预防组系列:与先水后氟(水—氟)对照组比,先低硒后氟组(低硒—氟)GSH-Px、SOD活力显著升高(P<0.05);先中硒后氟组(中硒—氟)GSH-Px活力显著升高(P<0.05);各先硒后氟组MDA含量均显著降低(P<0.05)。(2)治疗组系列:与先氟后水(氟—水)对照组比,先氟后低硒组(氟—低硒)和先氟后高硒组(氟—高硒)GSH-Px活力显著升高(P<0.05);先氟后中硒组(氟—中硒)SOD活力显著升高(P<0.05);各先氟后硒组MDA含量均显著降低(P<0.05)。结论硒对氟中毒致大鼠肝脏损伤有一定的干预作用,预防效果好于治疗效果,其中0.375mg/L是本实验条件下硒对慢性氟中毒致大鼠肝脏损伤的最佳预防作用浓度。
Objective To investigate the effect of selenium on liver injury induced by fluorosis in rats. Methods Different ways (first fed 0.375, 0.75 and 1.5mg / L sodium selenite solution for 6 months, then fed 50mg / L sodium fluoride solution for 6 months or first fed 50mg / L sodium fluoride solution 6 months, and then were fed 0.375,0.75 and 1.5mg / L sodium selenite solution for 6 months) rats were fed to observe the histopathology of rat liver, and determination of hepatic glutathione peroxidation (GSH-Px), superoxide dismutase (SOD) and malondialdehyde (MDA) and nuclear factor kappa B (NF-κB) Results Compared with the control group, the activities of GSH-Px and SOD in low-selenium-fluorine group were significantly lower than those in the control group (P <0.05) The content of GSH-Px in selenium-fluoride group increased significantly (P <0.05) after selenium exposure in selenium group. The content of malondialdehyde in selenium group decreased significantly (P <0.05). (2) In the treatment group, the GSH-Px activity of fluoride-low selenium group and fluoride-high selenium group after pre-fluoride post-fluoride selenium group was higher than that of the fluoride- (P <0.05). The content of MDA in selenium group (fluorine-selenium) was significantly increased (P <0.05). Conclusion Selenium has some effects on hepatic injury caused by fluoride poisoning in rats, and the preventive effect is better than that of the therapeutic effect. Among them, 0.375mg / L is the best preventive effect concentration of selenium on liver injury induced by chronic fluorosis in this experiment.