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目的观察短期碘摄入量异常对大鼠甲状腺滤泡上皮细胞凋亡及凋亡相关基因Bcl-2、Bax蛋白水平的表达及其在不同时间段不同性别中的表达差异。方法 90只Wistar大鼠随机分为低碘组、正常组和高碘组,雌雄各半,通过饮食饮水控制使各组碘摄入量分别为0.6μg/d、6.15μg/d和61.5μg/d。分别在饲养7、14和28 d后,处死动物并分离甲状腺。HE染色,光镜下进行形态学观察;免疫组化染色,MIAS-2000型图像分析系统观察分析甲状腺细胞凋亡相关基因Bcl-2、Bax蛋白水平的表达。结果各时间段各组大鼠甲状腺滤泡上皮细胞均未检出细胞凋亡。Bcl-2、Bax在低碘组和正常组均为阴性表达,在高碘组的表达高于正常组,且有随时间延长而有增强的趋势,其中,14 d时Bax表达出现阳性;28 d时Bcl-2、Bax表达均为阳性且高于正常组(P均<0.01)。7、14 d时,高碘组Bax在两性别中均有表达,表达水平在两性别中无统计学差别;28 d时,高碘组Bcl-2、Bax表达水平雄性均高于雌性,且差别均有统计学意义(P均<0.01)。结论短期碘缺乏和碘过量均不引起细胞凋亡,短期碘缺乏对凋亡相关基因无明显影响,短期碘过量既可促进促凋亡基因表达亦可促进抑凋亡基因表达。性别因素对甲状腺细胞凋亡相关基因的表达存在一定的影响。
Objective To observe the expression of Bcl-2 and Bax protein in thyroid follicular epithelial cells and the expression of Bcl-2 and Bax in thyroid follicular epithelial cells in rats with abnormal expression of short-term iodine intake and their differences in different sexes at different time points. Methods Totally 90 Wistar rats were randomly divided into low iodine group, normal group and high iodine group. The iodine intake of each group was 0.6μg / d, 6.15μg / d and 61.5μg / d. Animals were sacrificed and thyroid glands isolated after 7, 14 and 28 days of feeding, respectively. HE staining and morphological observation under light microscope. Immunohistochemical staining and MIAS-2000 image analysis system were used to observe the expression of Bcl-2 and Bax protein in thyroid cells. Results No apoptotic thyroid follicular epithelial cells were detected in each group at each time point. The expression of Bcl-2 and Bax was negative in low iodine group and normal group, and higher in normal iodine group than in normal group. The expression of Bcl-2 and Bax tended to increase with time, of which Bax was positive on the 14th day. The expression of Bcl-2 and Bax were both positive and higher than those in normal group (all P <0.01). At 7 and 14 days, Bax in high iodine group was expressed in both sexes, and there was no significant difference between the two sexes. On the 28th day, the expression of Bax and Bax in high iodine group was higher than that in female The differences were statistically significant (all P <0.01). Conclusions Both short-term iodine deficiency and excessive iodine can not induce apoptosis. Short-term iodine deficiency has no obvious effect on apoptosis-related genes. Short-term iodine excess can promote both pro-apoptotic and pro-apoptotic genes. Sexual factors have some influence on the expression of thyroid apoptosis-related genes.