Abstract

To provide reference basis for the apoptosis of breast cancer cells and the carcinogenesis of breast cancer, the effects of 7,12-dimethylbenz(a)anthracene on apoptosis regulators Fas ligand and B-cell lymphoma-2 were investigated. In this study, 62 female C57BL/6 mice aged from 4 w to 6 w were randomly divided into control group and test group, with 31 mice in each group. The test group was given 7,12-dimethylbenz(a) anthracene solution by gavage at a dose of 50 mg/kg and the control group was given normal saline of equal volume. On the 2nd d after the experiment, all the mice were killed by cervical dislocation. The results showed that after hematoxylin-eosin staining, the tumor cells in the test group were stacked up to form a substantial structure. The expression level of Fas ligand protein in the control group was greatly lower than that in the test group and the positive rate was 20.25 %, which was greatly lower than that of 89.65 % in the test group (p<0.01). The expression level of B-cell lymphoma-2 protein in the mammary gland tissues of mice in the test group was greatly higher than that of the control group and its positive rate was 87.96 %, which was greatly higher than that of 31.48 % in the control group (p<0.01). The expression levels of Fas ligand messenger ribonucleic acid in the mammary gland tissues of mice in the test group and control group were 5.82±4.37 and 1.27±0.12, respectively and there was a statistically obvious difference (p<0.05). The messenger ribonucleic acid expression levels of B-cell lymphoma-2 in the test group and the control group were 18.97±2.65 and 2.02±0.54, respectively, and there was an extremely obvious difference (p<0.01). The apoptosis rate of mammary gland cells in the test group was (19.79±3.53) % and that in the control group was (2.93±0.28) % and there was an extremely obvious difference (p<0.01). It indicated that 7,12-dimethylbenz(a)anthracene inhibited the apoptosis of breast cancer cells by regulating the upregulation of Fas ligand and B-cell lymphoma-2 expression.

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