The Role and Significance of Bcl-2 and Bax in the Hepatic Carcinoma
This study aimed to observe the regularity of liver cell apoptosis and expression of apoptosis related gene Bcl-2 and Bax in the induced cancer, and explore the relationship between apoptosis and the development of liver cancer. In this study, 84 rats were used, 72 rats as experimental group induced...
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| Autores principales: | , , , , , |
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| Lenguaje: | English |
| Publicado: |
Sociedad Chilena de Anatomía
2012
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| Materias: | |
| Acceso en línea: | http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0717-95022012000400032 |
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| Sumario: | This study aimed to observe the regularity of liver cell apoptosis and expression of apoptosis related gene Bcl-2 and Bax in the induced cancer, and explore the relationship between apoptosis and the development of liver cancer. In this study, 84 rats were used, 72 rats as experimental group induced by drinking water containing DEN, 12 rats as control group (CG). After laparotomy, the form, color, texture of the liver and metastatic tumor in both control and experimental groups were observed and recorded. The metastatic tumor and the liver tissue were sectioned and stained with hematoxylin-eosin staining to demonstrate the characteristic in morphological changes, the Hoechst 33342 fluorescent staining was applied to show and count the rate of apoptotic cell, and the in situ hybridization technique was used to detect the Bcl-2 and Bax expression. The results showed that the process of carcinogenesis can be divided into three periods: hepatic toxic lesion, hepatic proliferation/cirrhosis and hepatic carcinogenesis. The Hoechst 33342 fluorescent staining showed that the rate of apoptosis in the CG, hepatic toxic lesion, hepatic proliferation/cirrhosis and hepatic carcinogenesis were 6.7%,18.8%,17.4% and 51.2% c2=33.62, P<0.05 respectively. In situ hybridization showed the yellow positive reaction products of Bcl-2 and Bax located in the nucleus and cytoplasm of cell in diffusive distribution. The average optical densities of Bcl-2 and Bax expression were 0.1697±0.0101 and 0.1383±0.0093 in the control group, 0.1431±0.0072 and 0.1523±0.0103 in hepatic toxic lesion, 0.1261±0.0164 and 0.1639±0.0133 in hepatic proliferation/cirrhosis, 0.1034± 0.0124 and 0.1785±0.0191 in hepatic carcinogenesis, indicating that the expression of Bcl-2 decreased, but that of Bax increased with the development of liver cancer in experimental groups. In DEN induced liver cancer, the origination and development of liver cancer were accompanied with proliferation and abnormal apoptosis, which was related to the abnormal expression of gene Bcl-2 and Bax. |
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