高效氯氰菊酯对小鼠卵巢生殖功能的影响及维生素E的干预作用

为探究高效氯氰菊酯 (beta-cypermethrin, β-CP) 对雌性小鼠卵巢生殖功能的影响及维生素E (vitamin E, VE) 的干预作用，将雌性昆白小鼠随机分为6 组:空白对照组 (花生油处理)、β-CP不同剂量 (10、20、40 mg/kg) 处理组、VE保护组 (20 mg/kg β-CP+20 mg/kg VE) 和VE组 (20 mg/kg VE)，连续灌胃10 d。灌胃结束后取小鼠卵巢组织，观察组织结构的病理变化，采用免疫组化法、蛋白免疫印迹试验及RT-PCR方法检测卵巢中StAR蛋白含量及casp-3、casp-8、INHα和INHβB 基因mRNA表达的变化。结果显示:与对照相比，10、20和40 mg/kg的β-CP处理均使小鼠卵巢组织结构发生了损伤，使组织中StAR蛋白的浓度分别降低了18.8%、36.3%和40.3%，casp-3基因的表达分别升高了16.0%、26.7%和52.9%，INHα基因的表达分别升高了34.5%、83.6%和228.7%，INHβB基因的表达分别升高了7.5%、39.2%和52.7%；20和40 mg/kg的β-CP处理使得casp-8基因的表达分别升高了27.1%和36.7%。上述处理组与对照组的差异均达显著水平 (P＜0.05)。与 20 mg/kg β-CP处理组相比，VE 保护组的StAR蛋白含量也显著增多 (P＜0.05)。研究表明，β-CP对小鼠卵巢具有毒性作用，这与β-CP抑制StAR蛋白的合成，上调casp-3、casp-8、INHα及INHβB基因的表达有关；添加VE对小鼠卵巢有一定的保护作用，这与VE可减弱β-CP对StAR蛋白合成的抑制作用有关。

Influence of beta-cypermethrin and intervention effects of vitamin E on reproductive function of mice ovary

The study was conducted to investigate the influence of beta-cypermethrin (β-CP) on ovary reproductive function and the intervention of vitamin E (VE) in mice. Blank control (peanut oil treatment), three different doses of β-CP (10, 20 and 40 mg/kg), protection (20 mg/kg β-CP+20 mg/kg vitamin E) and vitamin E (20 mg/kg) were applied to 6 groups of mice for 10 d continuously. After the treatment, the ovarian tissue was obsoleted to observe the pathological changes of ovarian tissue structure. The changes of StAR protein content, casp-3, casp-8, INHα and INHβB gene expression were determined by immunocytochemistry, Western blotting and RT-PCR. The results showed that, compared with the control group, the treatment of β-CP at 10, 20 and 40 mg/kg damaged the ovarian tissue in mice, the concentration of StAR protein was reduced by 18.8%, 36.3% and 40.3%, the expression of casp-3 was increased by 16.0%, 26.7% and 52.9%, the expression of INHα was increased by 34.5%, 83.6% and 228.7%, the expression of INHβB was increased by 7.5%, 39.2% and 52.7%; the treatment of β-CP at 20 and 40 mg/kg increased the expression of casp-8 by 27.1% and 36.7%. There are significant differences between the above treatment groups and control groups (P < 0.05). The concentrarion of StAR protein increased in the protection group compared with the 20 mg/kg β-CP treatment group (P < 0.05). Those results demonstrated that β-CP had a toxic effect on the ovarian tissue of mice, which was caused by the inhibition of StAR protein synthesis by β-CP and the increase in the expression of casp-3, casp-8, INHα and INHβB. Vitamin E had a protection effect on mice ovarian tissue after, which resulted from the decrease of the inhibit effect of β-CP on StAR protein by vitamin E.