硒对高氟所致兔血管内皮损伤及动脉硬化影响的病理形态学研究

目的 研究硒对高氟所致兔动脉血管内皮细胞损伤和动脉硬化病理形态学变化的影响作用.方法 20只健康雄性新西兰白兔,体质量(2.0±0.5)kg,按体质量随机分对照组(饮去离子水,饲基础饲料)、加氟组(饮含氟离子100mg/L去离子水,饲基础饲料)、加硒组(饮含硒1 mg/L去离子水,饲基础饲料)、加氟加硒组(饮含氟离子100 mg/L、含硒1 mg/L去离子水,饲基础饲料),每组5只,实验期6个月.于实验第0、3、6个月取血测定血清含氟量和含硒量;实验终末取胸主动脉,观察主动脉病理及超微结构变化.结果实验第3、6个月时,加氟组和加氟加硒组血清氟(0.589±0.146)、(0.772±0.175)mg/L和(0.502±0.094)、(0.693±0.158)mg/L]显著高于对照组(0.174±0.002)、(0.208±0.031)mg/L,P均＜0.01];加氟组第6个月血清氟显著高于第3个月(P＜0.05).实验第3、6个月时,加硒组和加氟加硒组血清硒(0.252±0.022)、(0.319±0.052)mg/L和(0.239±0.016)、(0.294±0.018)mg/L]显著高于对照组(0.135±0.014)、(0.167±0.019)mg/L,P均＜0.01];加硒组第6个月血清硒显著高于第3个月(P＜0.05).对照组、加氟组、加硒组、加氟加硒组内皮细胞凋亡指数分别为(4.92±1.32)%、(30.30±6.80)%、(6.57±2.14)%和(14.29±2.99)%,氟与硒各自的主效应有统计学意义(F值分别为106.833、20.082,P均＜0.01),高氟与适硒之间存在显著的拮抗作用(F=30.402,P＜0.01).病理观察加氟组主动脉内皮有红细胞及纤维蛋白沉着,细胞走向及结构发生改变,血管受损严重;加氟加硒组减少内皮细胞凋亡,附着的纤维蛋白以及红细胞数量减少,内皮细胞结构基本正常,血管受损程度和范围明显减轻.结论适量硒抑制高氟引起的内皮细胞凋亡,减轻高氟所致主动脉结构破坏,保持内皮细胞的完整性,以此拮抗高氟对血管的损伤和促动脉粥样硬化作用.

Pathological morphology of vascular endothelial injury and arteriosclerosis caused by high fluoride and the effects of selenium

Objective To study morphological changes of rabbit artery endothelial cell injury and atherosclerosis caused by high fluoride and the role of selenium. Methods Twenty healthy male New Zealand white rabbits, body weight (2.0 ± 0.5)kg, were randomly divided into control group(drinking deionized water, fed basic diet), fluoride group(drinking fluoride 100 mg/L deionized water, fed basic diet), selenium group(drinking selenium 1 mg/L deionized water, fed basic diet), fluoride plus selenium group(drinking fluoride 100 mg/L deionized water, selenium 1 mg/L of deionized water, fed basic diet). The experimental period was 6 months. At 0, 3, 6 months of the experiment, serum fluorine and selenium levels were determined. At the end of the experiment,thoracic aorta was collected to observe its pathology and ultrastructural changes. Results Serum fluoride was significantly higher at the 3rd and the 6th month of experiment(all P ＜ 0.01 ) in fluoride group (0.589 ± 0.146),(0.772 ± 0.175)mg/L] and fluoride plus selenium group (0.502 ± 0.094), (0.693 ± 0.158)mg/L] than in control group (0.174 ± 0.002), (0.208 ± 0.031 )mg/L] and serum fluoride was significantly higher at 6 months than at 3 months(P ＜ 0.05 ) in fluoride group. Serum selenium was significantly higher at the 3rd and the 6th month of experiment (all P ＜ 0.01 ) in selenium group (0.252 ± 0.022), (0.319 ± 0.052)mg/L] and fluoride plus selenium group (0.239 ±0.016), (0.294 ± 0.018)mg/L] than in control group(0.135 ± 0.014), (0.167 ± 0.019)mg/L], and serum selenium was significantly higher at the 6th month than at 3rd month of experiment in selenium group(P ＜ 0.05). Endothelial cell apoptosis indices were (4.92 ± 1.32)%, (30.30 ± 6.80)%, (6.57 ± 2.14)% and (14.29 ± 2.99)%, respectively in control group, fluoride group, selenium group and fluoride plus selenium group. Their main effect of fluorine and selenium was statistically significant (F = 106.833,20.082, all P ＜ 0.01 ). There were antagonistic effect between fluoride and selenium(F = 30.402, P ＜ 0.01 ). Pathological changes of rabbit aortic endothelial cells in fluoride group included endothelial with attached fibrin and red blood cells, and structural of the cells changed, with serious vascular injury; in fluoride plus selenium group apoptosis of endothelial cells decreased, with reduced number of attached red blood cells and fibrin, endothelial cell structure normal, the extent and scope of vascular damage significantly reduced. Conclusions Appropriate amount of selenium inhibits the apoptosis of endothelial cells induced by high fluoride, reduces aortic structural damage caused by high fluoride, and maintains the integrity of endothelial cells, thereby antagonizes the vascular damage and atherosclerosis induced by high fluoride.