摘要
Objective： To observe the intervention effect of Shugan Jianpi Formula （疏肝健脾方,SGJPF） on a breast cancer mouse model with depression and investigate the underlying mechanism of SGJPF in preventing the development of breast cancer. Metkods： The breast cancer model was induced by inoculation of breast cancer cells, the depression model was induced by chronic stress stimuli, and the depression cancer model was established by combining the two factors. The mice were divided into 7 groups： normal control, depression model, tumor model, depression tumor model, SGJPF, chemotherapy, and SGJPF＋chemotherapy groups. The last 3 groups were depression breast cancer mice and treated respectively with SGJPF, chemotherapy drug gemcitabine （GEM）, and SGJPF alongside GEM. The condition of the mice was evaluated by the expression of 5-hydroxytryptamine in hippocampus after the sucrose water test and open field test, weight change, and survival time. Tumor growth was monitored with in vivo imaging. Flow cytometry was used to analyze the level of myeloid-derived suppression cell （MDSC） in the mouse spleen, T cell subsets, and the early apoptosis of CD8~ T cells, Results： The SGJPF＋GEM group had the highest inhibition rate and the longest survival time （P〈0.01）. The MDSC level and the apoptosis rate of CD8＊ T cells was the highest in the SGJPF＋GEM group （P〈0.05）. Conclusions： Depressive disorders and tumor growth could suppress the immune function of mice to different degrees, and the microenvironment in late 4T1 inflammatory breast cancer may play an important role in the pathological process. SGJYF could regulate the immune microenvironment by reducing CD8＊ T lymphocyte apoptosis and tumor cell activity, increasing immune surveillance capability, and inhibiting MDSC proliferation, thus prolonging the survival time of tumor-bearing mice.
Objective： To observe the intervention effect of Shugan Jianpi Formula （疏肝健脾方,SGJPF） on a breast cancer mouse model with depression and investigate the underlying mechanism of SGJPF in preventing the development of breast cancer. Metkods： The breast cancer model was induced by inoculation of breast cancer cells, the depression model was induced by chronic stress stimuli, and the depression cancer model was established by combining the two factors. The mice were divided into 7 groups： normal control, depression model, tumor model, depression tumor model, SGJPF, chemotherapy, and SGJPF＋chemotherapy groups. The last 3 groups were depression breast cancer mice and treated respectively with SGJPF, chemotherapy drug gemcitabine （GEM）, and SGJPF alongside GEM. The condition of the mice was evaluated by the expression of 5-hydroxytryptamine in hippocampus after the sucrose water test and open field test, weight change, and survival time. Tumor growth was monitored with in vivo imaging. Flow cytometry was used to analyze the level of myeloid-derived suppression cell （MDSC） in the mouse spleen, T cell subsets, and the early apoptosis of CD8~ T cells, Results： The SGJPF＋GEM group had the highest inhibition rate and the longest survival time （P〈0.01）. The MDSC level and the apoptosis rate of CD8＊ T cells was the highest in the SGJPF＋GEM group （P〈0.05）. Conclusions： Depressive disorders and tumor growth could suppress the immune function of mice to different degrees, and the microenvironment in late 4T1 inflammatory breast cancer may play an important role in the pathological process. SGJYF could regulate the immune microenvironment by reducing CD8＊ T lymphocyte apoptosis and tumor cell activity, increasing immune surveillance capability, and inhibiting MDSC proliferation, thus prolonging the survival time of tumor-bearing mice.
基金
Supported by the National Natural Science Foundation of China(No.81273946 and No.81072802)
the National Science and Technology Major Projects for"Major New Drugs Innovation and Development"(No.2013ZX09303301)
