国际医药卫生导报 ›› 2022, Vol. 28 ›› Issue (16): 2311-2315.DOI: 10.3760/cma.j.issn.1007-1245.2022.16.022

• 基础研究 • 上一篇    下一篇

双去甲氧基姜黄素对小鼠乳腺癌的抗肿瘤作用及机制

李学瑛1  徐阳2  王秘1   

  1. 1滨州职业学院健康学院,滨州 256600;2上海市医药学校生物技术制药系,上海 200135
  • 收稿日期:2022-04-25 出版日期:2022-08-15 发布日期:2022-08-15
  • 通讯作者: 李学瑛,Email:1165799376@qq.com

Effect and mechanism of bisdesmethoxycurcumin on breast cancer in mice

Li Xueying1, Xu Yang2, Wang Mi1   

  1. 1 School of Health, Binzhou Polytechnic, Binzhou 256600, China; 2 School of Biotech Pharmaceuticals, Shanghai Pharmaceutical School, Shanghai 200135, China
  • Received:2022-04-25 Online:2022-08-15 Published:2022-08-15
  • Contact: Li Xueying, Email: 1165799376@qq.com

摘要: 目的 本研究旨在研究双去甲氧基姜黄素(bisdesmethoxycurcumin,BDMC)对小鼠乳腺癌的影响及机制。方法 采用小鼠乳腺癌4T1细胞,分为Control组及不同剂量(3、9、27 μM)BDMC组,通过CCK8法检测BDMC对小鼠乳腺癌4T1细胞增殖的影响,TUNEL染色检测BDMC对4T1细胞凋亡的影响,Western blot检测BDMC对4T1细胞Bax、Bcl-2及cleaved caspase-3表达的影响;采用4T1乳腺癌荷瘤小鼠模型,分为Control组及不同剂量(10、30 mg/kg)BDMC组,检测BDMC对小鼠肿瘤体积及体质量的影响,Western blot检测BDMC对乳腺癌小鼠肿瘤组织Bax、Bcl-2及cleaved caspase-3表达的影响。采用单因素方差分析。结果 与Control组相比,9、27 μM BDMC均能明显抑制4T1细胞增殖(均P<0.01),促进其凋亡(均P<0.01),同时上调细胞Bax/Bcl-2比值及cleaved caspase-3表达(均P<0.01);10、30 mg/kg BDMC均能明显抑制乳腺癌小鼠肿瘤体积的增长(均P<0.05),同时明显上调肿瘤组织Bax/Bcl-2比值及cleaved caspase-3表达(均P<0.05),但对体质量无明显影响。结论 BDMC对乳腺癌小鼠模型具有明显的抗肿瘤作用,其机制与激活线粒体凋亡通路有关。

关键词: 双去甲氧基姜黄素, 乳腺癌, 增殖, 凋亡

Abstract: Objective To investigate the effect and mechanism of bisdesmethoxycurcumin (BDMC) on breast cancer in mice. Methods Mouse breast cancer 4T1 cells were used and were divided into a control group and 3, 9, and 27 μM BDMC groups. The effect of BDMC on the proliferation of mouse breast cancer 4T1 cells was detected by CCK8 assay, the effect of BDMC on the apoptosis of 4T1 cells was detected by TUNEL staining, and the effects of BDMC on the expressions of Bax, Bcl-2, and cleaved caspase-3 in 4T1 cells were detected by Western blot. The 4T1 breast cancer tumor-bearing mouse models were used and were divided into a control group and 10 and 30 mg/kg BDMC groups. The effects of BDMC on tumor volume and body weight of mouse models were detected, and the effects of BDMC on the expressions of Bax, Bcl-2, and cleaved caspase-3 in tumors were detected by Western blot. One-way ANOVA was used. Results Compared with the control group, BDMC at 9 and 27 μM could significantly inhibit the proliferation of 4T1 cells (both P<0.01), promote the apoptosis (both P<0.01), and significantly up-regulate the ratio of Bax/Bcl-2 and expression of cleaved caspase-3 (all P<0.01). Compared with the control group, BDMC at 10 and 30 mg/kg could significantly inhibit the growth of tumor volume in mouse models of breast cancer (both P<0.05), significantly up-regulate the ratio of Bax/Bcl-2 and expression of cleaved caspase-3 in tumor (all P<0.05), and had no significant effect on the body weight. Conclusion BDMC can exert significant antitumor effect on mouse models of breast cancer, and its mechanism is related to the activation of mitochondrial apoptosis pathway.

Key words: Bisdesmethoxycurcumin, Breast cancer, Proliferation, Apoptosis