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目的探讨氟致大鼠肾损伤的分子机制。方法将大鼠分为对照组和自由饮用氟化钠溶液低、中、高(15,30,60 mg/L)4组;9个月后处死大鼠,测定肾脏抗氧化水平和核因子κB(NF-κB)的表达量。结果低、高氟组丙二醛(MDA)含量与谷胱甘肽过氧化物酶(GSH-Px)活性分别为(1.61±0.18),(1.63±0.26)nmol/mg.prot和(11.39±1.38),(6.86±0.99)U/mg.prot,明显高于对照组(P<0.05);各染氟组超氧化物歧化酶(SOD)活性虽有下降趋势,但差异无统计学意义(P>0.05);随着染毒剂量加大,NF-κB表达量呈上升趋势,与对照组(0.136±0.024)比较,高氟组(0.178±0.019)明显升高(P<0.05)。结论慢性氟中毒可致大鼠肾脏组织氧化损伤。
Objective To investigate the molecular mechanism of renal injury induced by fluorine in rats. Methods Rats were divided into control group and low, medium and high (15, 30 and 60 mg / L) sodium fluoride groups. After 9 months, the rats were sacrificed and the renal antioxidant capacity and nuclear factor κB (NF-κB) expression levels. Results Low and high fluoride group malondialdehyde (MDA) content and glutathione peroxidase (GSH-Px) activity were (1.61 ± 0.18), (1.63 ± 0.26) nmol / mg.prot and (11.39 ± 1.38) and (6.86 ± 0.99) U / mg.prot, respectively, which were significantly higher than that of the control group (P <0.05). Although the activity of superoxide dismutase (SOD) in each fluoride group showed a downward trend, the difference was not statistically significant P> 0.05). The expression of NF-κB increased with the increase of exposure dose. Compared with the control group (0.136 ± 0.024), the high fluoride group (0.178 ± 0.019) increased significantly (P <0.05). Conclusion Chronic fluorosis can cause oxidative damage in rat kidney.