Carcinogenesis and Ito cell

癌变与伊藤细胞

基本信息

批准号：
08670598
负责人：
SAKAIDA Isao
金额：
$ 1.41万
依托单位：
Yamaguchi University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1996
资助国家：
日本
起止时间：
1996 至 1998
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-08670598/
关键词：
Ito cell Cancer Fibrosis Preneoplastic lesion TGF-beta1 肝発癌発癌

项目摘要

Administration of a choline deficient L-amino acid defined (CDAA) diet for 16 weeks led to the development of preneoplastic lesions that were positive for the placental form of glutathione S-transferase (GSTP) and induced hepatocellular carcinoma in 90% of rats after one year. Prolyl 4-hydroxylase inhibitor (HOE 077, 200 ppm) significantly reduced the size and incidence of preneoplastic lesions after 16 weeks and also the incidence of HCC (50%) in rats fed a CDAA diet for one year by the inactivation of Ito cell resulting in the prevention of fibrosis.Injection of pig serum into rats twice a week for 8 weeks induced.TGF-beta_1 mRNA expression and protein production resulting in liver fibrosis without parenchymal cell injury. Administration of a choline deficient L-amino acid defined (CDAA) diet for 6 weeks with or without pig serum pretreatment led to the development of preneoplastic lesions that were positive for the placental form of glutathione S- transferase (GSTP). Pig serum pretreatment induced more activated stellate cells with increased TGF-beta_1, mRNA expression and protein production in the livers of rats subsequently fed a CDAA diet for 6 weeks compared to rats fed the CDAA diet alone.These results indicate that pre-existing fibrosis with the activated stellate cells accelerates the development of preneoplastic lesions in a CDAA.diet model and that TGF-beta_1 induced by pig serum treatment failed to prevent the development of preneoplastic lesions in a CDAA-diet model.Cancer cell seems to prevent the activation of Ito cell in co-culture system but further examinations are necessary.

给药16周的胆碱缺乏的L-氨基酸定义（CDAA）饮食导致了麦芽糖化剂S-转移酶（GSTP）的胎盘形式呈阳性的肿瘤性病变的发展，并诱导的肝细胞癌在90％的大鼠中均为肝细胞癌年。脯氨酰4-羟化酶抑制剂（HOE 077，200 ppm）显着降低了16周后的肿瘤性病变的大小和发生率，并且由于ITO细胞的失活而在CDAA饮食中的HCC（50％）的发生率（50％）降低了一年在预防纤维化中，猪血清每周两次注射猪血清诱导8周。TGF-BETA_1 mRNA表达和蛋白质产生，导致肝纤维化无实质性细胞损伤。在有或没有猪血清预处理的情况下，施用胆碱缺乏的L-氨基酸（CDAA）饮食6周，导致牙骨质病变的发展，这些病变对谷胱甘肽S-转移酶（GSTP）的胎盘形式呈阳性。与单独喂食CDAA饮食相比活化的星状细胞加速了cdaa.diet模型中肿瘤性病变的发展，并且猪血清处理诱导的TGF-BETA_1无法阻止CDAA-DIET模型中质量塑性病变的发展。CANCANCER细胞似乎可以防止ITO的激活激活共培养系统中的细胞，但需要进一步检查。