Nanobacteria promotes apoptosis in breast cancer cell line MDA-MB-231

刘胜男; 张德纯; 张名均; 郭亚楠; 杨晓容; 许舸

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Nanobacteria promotes apoptosis in breast cancer cell line MDA-MB-231

更新时间：2026-01-09

- Nanobacteria promotes apoptosis in breast cancer cell line MDA-MB-231
- Journal of Army Medical University Vol. 35, Issue 16, Pages: 1688-1691(2013)
- 作者机构：
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  CLC： R318.08;R73-354;R737.9
- Published：2013
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刘胜男,张德纯,张名均,郭亚楠,杨晓容,许舸.纳米细菌促进乳腺癌细胞MDA-MB-231凋亡[J].陆军军医大学学报(原第三军医大学学报),2013,35(16):1688-1691.

　Liu Shengnan,Zhang Dechun,Zhang Mingjun,Guo Yanan,Yang Xiaorong,Xu Ke.Nanobacteria promotes apoptosis in breast cancer cell line MDA-MB-231[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(16):1688-1691.
刘胜男,张德纯,张名均,郭亚楠,杨晓容,许舸.纳米细菌促进乳腺癌细胞MDA-MB-231凋亡[J].陆军军医大学学报(原第三军医大学学报),2013,35(16):1688-1691. DOI：

　Liu Shengnan,Zhang Dechun,Zhang Mingjun,Guo Yanan,Yang Xiaorong,Xu Ke.Nanobacteria promotes apoptosis in breast cancer cell line MDA-MB-231[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(16):1688-1691. DOI：

摘要

目的观察纳米细菌（nanobacteria

NB）与纳米羟基磷灰石颗粒(nano hydroxyapatite，nHAP)对乳腺癌MDA-MB-231细胞的影响。方法实验分为NB组、nHAP组和正常对照组，其中NB组和nHAP组悬液的浓度均为2麦氏浊度（M），正常对照组仅加培养基，与乳腺癌MDA-MB-231细胞共同培养24、48、72 h，通过CCK-8检测其对细胞的毒性作用；培养12、24、48、72 h，取上清，经全自动生化分析仪测定LDH活性；作用72 h，经流式细胞仪(flow cytometry

FCM)测定其凋亡率，透射电镜观察其超微结构的变化情况。结果 CCK-8显示，NB组24、48、72 h对细胞的抑制作用均强于nHAP组和正常对照组，差异有统计学意义（

0.01）；NB组LDH含量在24、48、72 h时均高于正常对照组，差异均有统计学意义（

0.05）；24、48、72 h均高于nHA组，但仅24、48 h有统计学差异（

0.05）。nHAP组LDH活性仅在72 h与正常对照组比较有统计学差异（

0.01）；72 h后NB组细胞凋亡率高于nHAP组，差异有统计学意义（

0.01）；透射电镜下观察，NB组可以看到胞质空泡样变，核固缩以及明显的凋亡小体，nHAP组未见明显异常。结论 NB可以抑制乳腺癌细胞的生长，促进其发生凋亡，其导致细胞凋亡的成分不仅仅是NB羟基磷灰石的外壳，也可能与NB的其他组分或代谢产物有关。

Abstract

Objective To determine the effect of nanobacteria (NB) and nano hydroxyapatite (nHAP) on breast cancer cells. Methods Breast cancer MDA-MB-231 cells were treated by 100 μg/mL nHAP with a turbidity of 2 M and NB at a same turbidity for 12

24 and 48 h

respectively. The MDA-MB-231 cells receiving no treatment served as normal control. CCK-8 assay was used to determine the toxic effect of NB and nHAP on t

he cells. The activity of lactate dehydrogenase (LDH) in the supernatant was measured after the treatment for 12

48 and 72h

respectively. In 72 h after the treatment

flow cytometry (FCM) was used to measure the apoptotic rates

and transmission electron microscopy (TEM) was employed to observe the ultrastructure of the cells. Results CCK-8 assay revealed that NB showed significantly stronger inhibition on the proliferation of MDA-MB-231 cells than nHAP treated and normal control cells after 24

48 and 72 hours’ treatment (

0.01). NB also resulted in significantly higher LDH activity than normal control after 24

48 and 72 hours’ treatment (

0.05). The activity level was still higher in NB treated cells than in nHAP treated ones

but there were statistical differences only in 24 and 48 hour’s treatment (

0.05). Significant difference was also found in the LDH levels between nHAP treatment cells and control cells in 72 h (

0.01). In 72 h after treatment

the apoptotic rates of the breast cancer cells were obviously higher in NB treated group than in nHAP treated group (

0.01). TEM displayed that the MDA-MB-231 cells in NB group had cytoplasmic cavities

karyopyknosis and obvious apoptotic bodies. But no such change was found in the cells in the nHAP group. Conclusion NB inhibits the growth and promotes the apoptosis in breast cancer cells. It is due to not only hydroxyl apatite shell components

but also other components or metabolic products of NB.

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