CAJ | 학술논문

目的:探讨甲状腺激素缺乏对大鼠胸腺细胞凋亡及其相关蛋白Bcl-2和Bax表达的影响.方法:采用放射免疫技术测定甲巯咪唑组仔鼠血清中三碘甲状腺原氨酸(T3)、四碘甲状腺原氨酸(T4)、促甲状腺激素(TSH)水平;应用光镜、透射电镜技术和共聚焦激光扫描显微镜观察胸腺组织细胞形态学改变;免疫组织化学法检测胸腺组织中Bcl-2和Bax蛋白的表达.结果:甲巯咪唑组仔鼠体小,行动迟缓,胸腺绝对质量明显低于对照组,差异有统计学意义.对照组大鼠血清中T3、 T4值均高于甲巯咪唑组,TSH值低于甲巯咪唑组.甲巯咪唑组胸腺组织中出现大量的凋亡细胞和凋亡小体.Bcl-2蛋白表达的平均光密度值低于对照组;胸腺组织中Bax蛋白表达的平均光密度值高于对照组.结论:甲状腺激素缺乏可抑制胸腺组织中Bcl-2蛋白的表达和促进Bax蛋白的表达,诱导大鼠胸腺细胞凋亡,促进胸腺退化.
목적:탐토갑상선격소결핍대대서흉선세포조망급기상관단백Bcl-2화Bax표체적영향.방법:채용방사면역기술측정갑구미서조자서혈청중삼전갑상선원안산(T3)、사전갑상선원안산(T4)、촉갑상선격소(TSH)수평;응용광경、투사전경기술화공취초격광소묘현미경관찰흉선조직세포형태학개변;면역조직화학법검측흉선조직중Bcl-2화Bax단백적표체.결과:갑구미서조자서체소,행동지완,흉선절대질량명현저우대조조,차이유통계학의의.대조조대서혈청중T3、 T4치균고우갑구미서조,TSH치저우갑구미서조.갑구미서조흉선조직중출현대량적조망세포화조망소체.Bcl-2단백표체적평균광밀도치저우대조조;흉선조직중Bax단백표체적평균광밀도치고우대조조.결론:갑상선격소결핍가억제흉선조직중Bcl-2단백적표체화촉진Bax단백적표체,유도대서흉선세포조망,촉진흉선퇴화.
Objective: To investigate effects of thyroid hormone deficiency on the expression of apoptosis gene Bcl-2 and Bax proteins of the thymus in rats. Methods: The pregnant rats were divided into an experimental group and a control group randomly. The pregnant rats were given 0.02% methimazole water from the 4~( th) day of pregnancy. All filial rats were sacrificed at postnatal day 40. The thymic weight and index were measured, and triiodothyronine (T3), tetraiodothyronine (T4) and thyroid-stimulating hormone (TSH) were determined by radioimmunoassay. The cell morphological changes in the thymus were observed by light microscopy, electronic microscopy and confocal laser scanning microscopy;immunohistochemical SP method was used to detect the expression of Bcl-2 and Bax in the thymus. Results: The filial rats of the experimental group were small and sluggish. The absolute weight of the thymus was significantly lower than that of the control group. The values of T3 and T4 in the serum of the experimental filial rats were both lower than those in the control rats, and the value of TSH in the serum of the experimental filial rats were both higher than that in the control rats. The morphological changes including compaction and margination of the nuclear chromatin, apoptotic bodies, and cell apoptosis were significantly increased in the experimental group. The average optical density of Bcl-2 protein expression in the experimental group was higher than that in the control group and that of Bax protein expression in the experimental group was lower than that in the control group. Conclusion: Thyroid hormones deficiency could inhibit the Bcl-2 protein expression, promote the Bax protein expression of the thymus tissue, and then induce the apoptosis and accelerate the degradation of thymus.