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[大鼠肝脏中卵圆细胞与2-乙酰氨基芴诱导的癌前病变之间的关系]

[Relationship between oval cells and preneoplastic lesions induced by 2-acetylaminofluorene in rat liver].

作者信息

Liao G, Chen J, Ding L

机构信息

Department of Pathology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & School of Basic Medicine, Peking Union Medical College, Beijing 100005.

出版信息

Zhonghua Bing Li Xue Za Zhi. 1998 Apr;27(2):87-90.

Abstract

OBJECTIVE

To study the cellular origin of preneoplastic lesion of liver induced by the 2-acetylaminofluorene (2-AAF) in rat.

METHODS

Male fisher 344 rats were used for two different carcinogenesis models. Model 1: Rats were fed with regular diet containing 0.02% 2-AAF for totally 28 days, and subjected to a standard two thirds partial hepatectomy (2/3 PH) on the 7th day in order to stimulate the proliferation of oval cells. 3H thymidine (3H-Tdr) was administered intraperitoneally on the 12th day for selective labelling of oval cells. Model II: Rats were subjected to 2/3 PH and 3H-Tdr was administered intraperitoneally 22 hours after the operation for the selective labelling of hepatocytes. The rats were then fed with 2-AAF for totally 28 days after a 9 days recovery period from 2/3 PH. The relationship between preneoplastic lesion and selectively labelled oval cells, or hepatocytes, was traced by autoradiography.

RESULTS

Pathological examination and autoradiography denoted that the silver grains (labelled signals) were only formed in the preneoplastic cells in model I rather than the cells of model II animals.

CONCLUSION

It is a direct evidence to demonstrate that the preneoplastic cells are mostly originated from the oval cells.

摘要

目的

研究2-乙酰氨基芴(2-AAF)诱导大鼠肝脏癌前病变的细胞起源。

方法

雄性Fisher 344大鼠用于两种不同的致癌模型。模型1:给大鼠喂食含0.02% 2-AAF的常规饲料,共28天,并在第7天进行标准的三分之二部分肝切除术(2/3 PH),以刺激卵圆细胞增殖。在第12天腹腔注射3H胸腺嘧啶核苷(3H-Tdr)以选择性标记卵圆细胞。模型II:大鼠接受2/3 PH,术后22小时腹腔注射3H-Tdr以选择性标记肝细胞。然后在大鼠从2/3 PH恢复9天后,给其喂食2-AAF,共28天。通过放射自显影追踪癌前病变与选择性标记的卵圆细胞或肝细胞之间的关系。

结果

病理检查和放射自显影表明,银颗粒(标记信号)仅在模型I的癌前细胞中形成,而在模型II动物的细胞中未形成。

结论

这是证明癌前细胞主要起源于卵圆细胞的直接证据。

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