|
Objective: endostatin on apoptosis of breast cancer cells in nude mice and Bcl-2, Bax in rats to explore the possible mechanism of action of endostatin. Method: 1. Establish nude mouse model of human breast cancer 30, were randomly divided into three groups of 10. 2 breast cancer cell suspensions were inoculated in the first week after planting site subcutaneous endostatin, every other day at doses of 10.0mg/kg (treatment group Ⅰ), 20.0mg/kg (treatment group Ⅱ) in the control group with PBS solution instead, sharing seven weeks. 3 The first 8 weeks mice were sacrificed by cervical dislocation and complete stripping cancer, detection of tumor volume, tumor inhibition rate of tumor microvessel density (MVD), apoptosis index (AI), liver and lung metastases and tumor cells Bcl-2, Bax expression. 4 using SPSS 12.0 statistical software for data processing. Result: a control group, the treatment group Ⅰ, group Ⅱ treatment tumor volume was (43.65 ± 0.64) cm ~ 3, (18.35 ± 0.67) cm ~ 3, (4.13 ± 0.58) cm ~ 3. The above data, the difference between groups was significant (P <0.05) .2. Control group, the treatment group Ⅰ, Ⅱ group therapy inhibition rates were 0,58.4%, 91.3%; MVD was (9.6 ± 1.2) , (4.6 ± 0.9), (1.8 ± 0.4). The above data, the difference between groups was significant (P <0.05) .3. Control group, the treatment group Ⅰ, group Ⅱ treatment liver (lung) metastasis rates were 90% (80%), 60% (50% ), 0, liver and lung metastasis rate of the treatment group Ⅱ compared with the control group, treatment group Ⅰ, the difference was statistically significant (P <0.05), while the treatment group Ⅰ compared with the control group, no statistical significance (P> 0.05). Four in the control group, the treatment group Ⅰ, group Ⅱ tumor AI treatment were (3.50 ± 0.94)%, (8.29 ± 2.60)%, (17.46 ± 4.50)%, the above data, the difference between groups was significant (P <0.05). 5 in the control group, the treatment group Ⅰ, group Ⅱ treatment of tumor cells Bcl-2 gray values ??were (0.90 ± 0.10), (0.70 ± 0.21), (0.41 ± 0.12), the above data, the difference between groups statistically significant (P <0.05). Six in the control group, the treatment group Ⅰ, Ⅱ group therapy Bax gray values ??were (0.51 ± 0.10), (0.50 ± 0.10), (0.55 ± 0.09), the above groups were not statistically significant (P> 0.05). 7 From the above data endostatin down nude Bcl-2 expression in breast cancer cells, had no effect on the expression of Bax, thereby changing the apoptosis regulatory proteins Bcl-2, Bax ratio in tumor cells promote tumor cell apoptosis, showing tumor volume decreases, the inhibition rate increased microvessel density (MVD) decreased apoptosis index (AI) increased, decreased liver and lung metastasis. Conclusion: Endostatin apoptosis of breast cancer is one of the molecular mechanisms of tumor cell resistance to apoptosis decreased Bcl-2 protein expression.
|