目的探讨氟中毒对肝纤维化的影响及其意义,并具体观察氟中毒对肝脏的形态学变化,了解其作用机制。方法采用C57小鼠氟化钠染毒模型,分为A、B、C 3个组,其中A组为实验组,根据饮水中含氟浓度分空白组(0 mg/L)、低剂量组(25 mg/L)、中剂量组(50 mg/L)、高剂量组(100 mg/L),普通饲料喂养6个月;B、C两组为干预组,时间为6个月,B组,前阶段喂养正常饲料,后38 d将亚硒酸钠加入饲料中,浓度为3 mg/kg;C组,前十周喂养正常饲料,第十一周开始喂养高脂、高糖饲料,饮水不变,喂养3 w高脂、高糖饲料。6个月后,取小鼠肝脏,分别使用HE染色和Masson胶原纤维特殊染色病理组织学检查,观察肝纤维化程度。结果 A、B和C组小鼠随着饮水含氟浓度的增加,其HE染色切片均显示肝细胞水肿加重;在相同含氟浓度的条件下A、B和C组小鼠中细胞水肿表现程度为:C组比A组严重,A组比B组严重;而Masson染色切片显示,A、B和C组实验小鼠随饮水含氟浓度的增加,汇管区和血管内皮的纤维结缔组织增生明显,肝脂肪细胞数量也逐渐增加;在相同含氟浓度的A、B和C组小鼠中:C组的纤维结缔组织增生和肝脂肪细胞数量增加最明显,其次A组比B组明显。结论氟中毒可以诱导肝脏发生纤维化,其中汇管区最为明显,其他部位也可见到纤维结缔组织增生,其中血管内皮纤维结缔组织增生也较为明显,而且随着饮水含氟浓度升高,其诱导肝脏发生纤维化的能力加大。 Objective To investigate the effect of fluorosis on liver fibrosis and its significance, and to observe the morphological changes of liver caused by fluorosis and to understand its mechanism. Methods C57 mouse sodium fluoride exposure model was divided into A, B, C three groups, of which A group was the experimental group, according to the concentration of fluoride in drinking water blank group (0 mg / L), low dose group 25 mg / L), medium dose (50 mg / L), high dose (100 mg / L) and normal diet for 6 months. Groups B and C were intervention groups with a time of 6 months. , The normal feed was fed in the previous stage, and then the sodium selenite was added to the feed at 38 days after the feed, at a concentration of 3 mg / kg. In the C group, the normal feed was fed in the first ten weeks and fed with high fat and sugar at the eleventh week Unchanged, fed 3 w high fat, high sugar feed. Six months later, the liver of the mice was taken, and the pathological changes of liver fibrosis were observed by HE staining and Masson collagen staining respectively. Results A, B and C groups of mice with He-stained sections showed increased hepatocyte edema with the increase of fluoride concentration in drinking water. The degree of cell edema in groups A, B and C at the same fluoride concentration : Group C was more severe than group A, and group A was more serious than group B. Masson staining showed that with the increase of fluoride concentration in drinking water, the connective tissues in portal area and vascular endothelium were significantly proliferated in group A, B and C , And the number of hepatic fat cells also increased gradually. In group A, B and C with the same fluoride concentration, the number of connective tissue hyperplasia and hepatic fat cell in group C increased most obviously. Conclusion Fluorosis can induce fibrosis in the liver, especially in the portal area. In other sites, fibrous connective tissue hyperplasia is also observed. The connective tissue hyperplasia is more obvious in the vascular endothelial fibers. And with the increase of fluoride concentration in the drinking water, the liver is induced The ability to fibrosis increases.