Growth inhibition and induction of apoptosis in MCF-7 breast cancer cells by oridonin nanosuspension

被引：35

作者：

Feng, Fei-Fei ^{[1
]}

Zhang, Dian-Rui ^{[1
]}

Tian, Ke-Li ^{[2
]}

Lou, Hai-Yan ^{[3
]}

Qi, Xiao-Li ^{[2
]}

Wang, Yan-Cai ^{[1
]}

Duan, Cun-Xian ^{[1
]}

Jia, Le-Jiao ^{[1
]}

Wang, Fei-Hu ^{[1
]}

Liu, Yue ^{[1
]}

Zhang, Qiang ^{[4
]}

机构：

[1] Shandong Univ, Dept Pharmaceut, Coll Pharm, Jinan 250012, Shandong, Peoples R China

[2] Shandong Univ, Inst Biochem & Mol Biol, Sch Med, Jinan 250012, Shandong, Peoples R China

[3] Shandong Univ, Dept Pharmacol, Sch Med, Jinan 250012, Shandong, Peoples R China

[4] Peking Univ, State Key Lab Nat & Biomimet Drugs, Sch Pharmaceut Sci, Beijing 100083, Peoples R China

来源：

DRUG DELIVERY | 2011年 / 18卷 / 04期

关键词：

Oridonin; nanosuspension; MCF-7; cells; apoptosis; LIPID NANOPARTICLES; BCL-2; DRUGS;

D O I：

10.3109/10717544.2010.536271

中图分类号：

R9 [药学];

学科分类号：

100702 [药剂学];

摘要：

The mechanism for anti-tumor activity of oridonin (ORI) nanosuspension, prepared by the high pressure homogenization method, was studied using MCF-7 human breast carcinoma cells in vitro. MTT assay, observation of morphologic changes, flow cytometric analysis, and western blot analysis indicated that ORI nanosuspension could significantly intensify the in vitro anti-tumor activity to MCF-7 cells, as compared with ORI solution. Furthermore, ORI nanosuspension induced G(2)/M stage proliferation arrest and apoptosis in MCF-7 cells depending on its concentration. In addition, western blot analysis indicated that the pro-caspase-3 protein was not cleaved into the activated form and the expression of anti-apoptotic Bcl-2 protein decreased, on the contrary, the expression of pro-apoptotic Bax protein increased in a dose-dependent manner in ORI nanosuspension-treated cells. These observations indicated that the anti-tumor activity of ORI nanosuspension was intensified by cell-cycle arrest and apoptosis induction.

引用

页码：265 / 271

页数：7

共 18 条

[1]

Regulation of p53 stability and activity in response to genotoxic stress [J].