| IntroductionPrimary hepatocarcinoma (PHC) is a commonly encountered clinical malignant tumor, whose incidence is the third in the olimentary system rumors, with a high death rate and poor prognosis. And it is called attention that the incidence rate of this rumor is increasing these years, and considered that the development and progression of primary hepatocarcinoma is relevant to the programmed cell death (PCD), and the initiation is probably caused by the loss of balance between the cell proliferation and death. However it is not fully understood about the biochemical mechanism of the development and progression of this tumor.Caspase-3 is one of the important ICE family members, the operator of PCD. Bcl-2 is the oncogene of follicular B-cell lymphoma. The [Bcl-2] can stop releasion of cytochrome C and restrict the activity of cpp-32, then restrain programmed cell death. In this study, immunohisto chemistry was used to detect the expression of Bcl-2 and caspase-3 in primary hepatocarcinoma and hepatocirrhosis (HC). We analyse the relationship between the expression level and clinical data for the purpose to understand the role of Bcl-2 and Caspase-3 in the occurrence and development of primary hepatocarcinoma. Materials and MethodsTo collect 42 specimens of primary hepatocarcinoma, 17 specimens of hepatocirrhosis placed on the file. For the primary hepatocarcinoma, there were 13 women and 29 men, with a mean age of 53.6 (range from 36 to 74). There were 20 better differentiated primary hepatocarcinoma and 22 poor differentiated primary hepatocarcinoma.Four-micrometer-thick sections were cut from formalin-fixed paraffin-embedded tissue blocked and mounted on polylysine-coated glass sliders. The positive controls were sections of Lymph node (Bcl-2) and tonsillar tissue(Caspase-3). Negative controls were sections stained without the primary antibody. Plasma that has immuno reactivity is yellow or brown. For each section, 10 high-power (×400) microscopic fields were examined for 94.10 cells. Bcl-2/ Caspase-3: greater than 10％of cells showed immunoreactivity(+); less than 10％of cells showed no immunoreactivity (-)The data were processed with the SPSS software applying chi-square test.ResultsFor the hepatocirrhosiss, 17 showed normal Caspase-3 expression. None showed Bcl-2 expression. For the 42 primary hepatocarcinoma, 19 showed normal Caspase-3 expression(45.2％). The rate of positive expression was significantly lower than that of hepatocirrhosis (P＜0.05). For the 42 primary hepatocarcinoma, 15showed normal Bcl-2 expression (35.7％). And the positive rate was significantly higher than that of hepatocirrhosis.For the 42 primary hepatocarcinoma, 15 showed normal Caspase-3 expression (45.2％). The positive rate was significantly higher in better-differentiated Os primary hepatocarrcinoma than that in lower-differentiated cases(P＜0.05). The rate of normal expression was not associated with gender and age.For the primary hepatocarcinoma, 15 showed normal Bcl-2 expression (35.7％). The positive rate was signifitantly higher in the better differentiated primary hepatocarcinoma than that in lower differentiated primary hepatocarcinoma, the rat was not associated with gender and age.For the 15 primary hepatocarcinoma that expressed normal Bcl-2 level, 13 showed normal Caspase-3 expression (92.9％); For the 27 primary hepatocarcinoma that expressed decreased Bcl-2 level, 22 showed decreased Caspase-3 expression (81.5％). The correlation was found between the Caspase-3 and the Bcl-2.ConclusionExpression of Bcl-2 in better differentiated primary hepatocarcinoma significantly high. This suggests that Bcl-2 restricts programmed cell death on early stage in primary hepatocarcinoma, and closely associated with occurrence of primary hepatocarcinoma. The down-regulation of Caspase-3 expression is a common event in primary hepatocarcinoma. So it is associated with occurrence and development of primary hepatocarcinoma. Caspase-3 and Bcl-2 were co-expressed in primary hepatocarcinoma. This suggests that, in primary hepatocarcinoma, the programmed cell death's restriction is a result of their mutual action. |
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