CAJ | 학술논문

目的：探讨外源性三碘甲状腺原氨酸（T3）对小鼠肝脏增生的影响。方法健康SPF级雌性C57BL/6小鼠45只，按随机数字表法随机分为A组、B组和对照组，每组15只。A、B组小鼠分别按每公斤体重10、5μg经腹腔内注射外源性T32 ml，对照组注射生理盐水2 ml。3组分别于处理后0、7、14、21、42 d时各处死3只小鼠。处死后测量小鼠全肝脏重量。采用免疫组织化学方法检测肝细胞增殖情况。实验数据间比较采用t检验或方差分析。结果与对照组相比，处理后7、14、21、42 d A组的肝脏重量明显增加（t=3.298，6.760，7.119，6.128；P<0.05），处理后14、21、42 d B组的肝脏重量明显增加（t=4.188，4.570，2.978；P<0.05）。处理后7、14、21、42 d A组增加的肝脏重量均比B组明显多（t=4.935，4.303，4.033，4.480；P<0.05）。其中处理后21 d，A、B组的肝脏重量增加至高峰（F=21.480，11.244；P<0.05）。与对照组相比，处理后0、7、14、21、42 d A组肝细胞数明显增加（t=28.383，23.842，40.194，31.059，15.841；P<0.05），B组的肝细胞数也明显增加（t=9.097，7.680，20.597，42.192，14.415；P<0.05）；且A组增加的肝细胞数均比B组明显多（t=8.016，4.872，10.719，9.514，7.831；P<0.05）。其中处理后14 d，A组的肝细胞数增加至高峰（F=169.190，P<0.05）；处理后21 d，B组的肝细胞数增加至高峰（F=90.460，P<0.05）。处理后A、B组肝细胞均发生广泛性增殖。结论外源性T3可有效促进小鼠肝脏增生，随着T3浓度的升高，增生更为明显。
목적：탐토외원성삼전갑상선원안산（T3）대소서간장증생적영향。방법건강SPF급자성C57BL/6소서45지，안수궤수자표법수궤분위A조、B조화대조조，매조15지。A、B조소서분별안매공근체중10、5μg경복강내주사외원성T32 ml，대조조주사생리염수2 ml。3조분별우처리후0、7、14、21、42 d시각처사3지소서。처사후측량소서전간장중량。채용면역조직화학방법검측간세포증식정황。실험수거간비교채용t검험혹방차분석。결과여대조조상비，처리후7、14、21、42 d A조적간장중량명현증가（t=3.298，6.760，7.119，6.128；P<0.05），처리후14、21、42 d B조적간장중량명현증가（t=4.188，4.570，2.978；P<0.05）。처리후7、14、21、42 d A조증가적간장중량균비B조명현다（t=4.935，4.303，4.033，4.480；P<0.05）。기중처리후21 d，A、B조적간장중량증가지고봉（F=21.480，11.244；P<0.05）。여대조조상비，처리후0、7、14、21、42 d A조간세포수명현증가（t=28.383，23.842，40.194，31.059，15.841；P<0.05），B조적간세포수야명현증가（t=9.097，7.680，20.597，42.192，14.415；P<0.05）；차A조증가적간세포수균비B조명현다（t=8.016，4.872，10.719，9.514，7.831；P<0.05）。기중처리후14 d，A조적간세포수증가지고봉（F=169.190，P<0.05）；처리후21 d，B조적간세포수증가지고봉（F=90.460，P<0.05）。처리후A、B조간세포균발생엄범성증식。결론외원성T3가유효촉진소서간장증생，수착T3농도적승고，증생경위명현。
Objective To investigate the impact of exogenous of triiodothyronine (T3) on the liver hyperplasia of mouse. Methods Forty-ifve healthy speciifc pathogen free (SPF) C57BL/6 mice were divided into group A, B and control group using random number table method with 15 mice in each group. Mice in group A, B were respectively injected with 2 ml exogenous T3 solutions 10, 5μg/kg intraperitoneally. Mice in control group were injected with 2 ml normal saline. Three mice of each group were put to death respectively on day 0, 7, 14, 21, 42 after treatment. The total liver weight of the mice was measured after death. The proliferation of liver cells was detected by immunohistochemistry. The experimental data were compared using t test or analysis of variance. Results Compared with control group, the liver weight of mice in group A increased signiifcantly on day 7, 14, 21, 42 after treatment (t=3.298, 6.760, 7.119, 6.128;P<0.05) , and the liver weight of mice in group B increased signiifcantly on day 14, 21, 42 after treatment (t=4.188, 4.570, 2.978;P<0.05). The increased liver weight in group A was signiifcantly more than that in group B on day 7, 14, 21, 42 after treatment (t=4.935, 4.303, 4.033, 4.480;P<0.05). The liver weight in group A, B rose to the top on day 21 after treatment (F=21.480, 11.244;P<0.05). Compared with control group, the liver cell count in group A increased signiifcantly on day 0, 7, 14, 21, 42 after treatment (t=28.383, 23.842, 40.194, 31.059, 15.841;P<0.05), and the same with group B (t=9.097, 7.680, 20.597, 42.192, 14.415;P<0.05). The increased liver cell count in group A was signiifcantly more than that in group B (t=8.016, 4.872, 10.719, 9.514, 7.831;P<0.05). The liver cell count rose to the top in group A on day 14 after treatment (F=169.190, P<0.05) and rose to the top in group B on day 21 after treatment (F=90.460, P<0.05). Extensive proliferation of liver cells was observed both in group A and B after treatment. Conclusions Exogenous T3 can effectively promotes the liver hyperplasia of mouse, and the hyperplasia becomes more signiifcant as the T3 concentration rises.