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目的:观察乳癌术后方对乳腺癌肺转移模型小鼠移植瘤生长的影响,探讨其可能的作用机制。方法:萤火虫荧光素酶标记的小鼠乳腺癌肺高转移细胞4T1(4T1-luc)接种于小鼠第三对乳房脂肪垫建立乳腺癌肺转移模型;于接种后7 d随机分组:NS组、扶正组、解毒组、全方组及环磷酰胺组,每组6只,连续给药21 d。计算肿瘤抑制率,以生物发光成像系统监测肿瘤细胞在体内的生长过程,通过肺转移灶定量分析观察小鼠肺转移情况,并采用蛋白印迹法(Western blotting)检测原位瘤中TLR4、NF-κB及IκB等蛋白的表达。结果:经过21 d给药,除了扶正组小鼠体重变化不明显,其余各组体重均有不同程度的降低。与NS组相比,各用药组瘤体积、肺转移抑制率均有所降低;全方组瘤体积、肺转移抑制率均较扶正组低(P<0.05),与解毒组相比仅瘤体积差异有统计学意义(P<0.05)。各组小鼠原位瘤组织中NF-κB蛋白表达水平无明显差异,但是与NS组相比,给药组的磷酸化的NF-κB蛋白(p-NF-κB)及磷酸化的IκB蛋白(p-IκB)均有明显降低,且全方组较扶正组、解毒组表达更低。另外,与NS组比较,乳癌术后方全方组及其拆方组IκB蛋白表达均有所上升,而TLR4蛋白表达水平均有所下降。结论:乳癌术后方对乳腺癌肺转移模型小鼠均有抑瘤和抗肿瘤转移作用,其机制可能与调节肿瘤微环境中TLR4/NF-κB通路相关蛋白表达有关。
Objective: To observe the effect of postoperative breast-cancer prescription on the growth of transplanted lung in mice with lung metastasis of breast cancer and to explore its possible mechanism. Methods: The mouse lung cancer cell line 4T1 (4T1-luc) labeled with firefly luciferase was inoculated on the third pair of mammary fat pad in mice to establish a lung metastasis model of breast cancer. At 7 days after inoculation, mice were randomly divided into NS group, Fuzheng group, detoxification group, the whole group and cyclophosphamide group, 6 in each group, continuous administration of 21 d. The rate of tumor inhibition was calculated. The growth of tumor cells in vivo was monitored by bioluminescence imaging system. Lung metastasis was observed by quantitative analysis of lung metastases. The expressions of TLR4 and NF-κB were detected by Western blotting. κB and IκB protein expression. Results: After 21 days of administration, body weight of mice in Fuzheng group was not significantly changed, and body weight of the other groups were decreased to some extent. Compared with the NS group, the tumor volume and the inhibition rate of lung metastasis were all decreased in all treatment groups. The tumor volume and lung metastasis inhibition rate in all treatment groups were lower than those in Fuzheng group (P <0.05) The difference was statistically significant (P <0.05). Compared with the NS group, the phosphorylation of NF-κB protein (p-NF-κB) and phosphorylated IκB protein of the mice in each group showed no significant difference (p-IκB) were significantly lower, and the whole group Fuzheng group, detoxification group lower expression. In addition, compared with the NS group, the expression of IκB protein was increased and the expression of TLR4 protein was decreased in the treated group and its subgroups. CONCLUSION: The mechanism of breast cancer after operation and postoperative administration on tumor-bearing lung cancer in breast cancer model mice may be related to the regulation of TLR4 / NF-κB pathway-related protein expression in tumor microenvironment.