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应用免疫组化方法观察小鼠肝脏癌前病变 P 16表达。将纯系津白 2小白鼠随机分三组 (每组 2 0只 ) :A组 ( AFB1 )、B组 ( AFB1 +香烟熏 )和 C组 (对照 )。同时选人体肝癌、肝结石和肝硬变相对比。AFB1 溶于 DMSO5 μg/日·只量拌于饲料投食 ,熏烟组以烟丝 3 0 g/日·只熏烟。经半年试验 ,处死动物 ,取肝脏行 HE染色同时进行本项实验。应用医学图像处理系统检测 P16蛋白表达强度。结果 P16蛋白表达强度分别为 :光密度均值 A组( 13 12 88.83 2 7) >B组 ( 10 9812 .812 2 ) >C组 ( 5 65 69.70 62 )。经 Q检验 ,P<0 .0 5 ,三组间均有差别。另外 ,肝癌( 19110 4 .5 879) >肝硬化 ( 1112 93 .9892 ) >结石 ( 5 5 663 .2 93 1)。反映 P16基因的突变或杂合子缺失 ,引起细胞增生的调控机制紊乱 ,细胞处于过度增生状态
Immunohistochemistry was used to observe the expression of P 16 in precancerous liver lesions of mice. The pure line Jinbai 2 mice were randomly divided into three groups (20 in each group): group A (AFB1), group B (AFB1 + cigarette smoked) and group C (control). At the same time, human liver cancer, liver stones, and cirrhosis were compared. AFB1 was dissolved in DMSO (5 μg/day) and was only added to the diet, while the smoked tobacco group was 30 g/day. After half a year of testing, the animals were sacrificed, and the livers were subjected to HE staining for this experiment. The medical image processing system was used to detect the intensity of P16 protein expression. Results The intensity of P16 protein expression was: the average optical density of group A (13 12 88.83 2 7)> group B (10 9812.812 2)> group C (5 65 69.70 62). After Q test, P<0.05, there were differences among the three groups. In addition, liver cancer (19110 4 .5 879)> cirrhosis (1112 93 .9892)> stones (5 5 663 .2 93 1). The P16 gene mutation or heterozygote deletion results in disordered regulation of cell proliferation and cells are in hyperproliferative state.