多柔比星-五味子乙素共载脂质体克服多药耐药的机制研究

杨建苗; 李天傲; 许东航<sup>*</sup>

引用本文:	杨建苗,李天傲,许东航.多柔比星-五味子乙素共载脂质体克服多药耐药的机制研究[J].中国现代应用药学,2017,34(12):1679-1682.
	YANG Jianmiao,LI Tian'ao,XU Donghang.Mechanism Study of Doxorubicin-schisandrin B Co-delivery Liposomes to Overcome Multidrug Resistance[J].Chin J Mod Appl Pharm(中国现代应用药学),2017,34(12):1679-1682.

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多柔比星-五味子乙素共载脂质体克服多药耐药的机制研究
杨建苗¹, 李天傲^2,3, 许东航²
1.台州恩泽医疗中心(集团)浙江省台州医院, 浙江临海 317000;2.浙江大学医学院附属第二医院, 杭州 310009;3.中国药学会, 北京 100022

摘要:

目的探讨多柔比星-五味子乙素共载脂质体克服肿瘤多药耐药机制。方法制备多柔比星-五味子乙素共载脂质体，以人慢性髓系白血病耐药细胞株K562/DOX为模型细胞，分别探讨不同温度、内吞抑制剂存在下的细胞摄取药物的情况，并检测耐药细胞P-gp表达和细胞凋亡情况。结果共载脂质体在4℃及氯喹、叠氮钠和甘露醇内吞抑制剂存在下进入耐药细胞的药物量明显减少；流式细胞仪检测多柔比星-五味子乙素共载脂质体可抑制P-gp表达且诱导凋亡。结论多柔比星-五味子乙素共载脂质体进入K562/DOX细胞主要通过耗能的内吞途径；而多柔比星-五味子乙素共载脂质体克服肿瘤多药耐药可能是通过抑制P-gp表达和促进凋亡双通道途径。

关键词: 多柔比星五味子乙素共载脂质体多药耐药机制

DOI：10.13748/j.cnki.issn1007-7693.2017.12.008

分类号:R965.2

基金项目:浙江省自然科学基金资助项目（LY15H300001，LY18H300004）；恩泽医疗中心（集团）科学研究基金资助项目（16EZD23）

Mechanism Study of Doxorubicin-schisandrin B Co-delivery Liposomes to Overcome Multidrug Resistance

YANG Jianmiao¹, LI Tian'ao^2,3, XU Donghang²

1.Taizhou Hospital of Zhejiang Province, Taizhou Enze Medical Center(Group), Linhai 317000, China;2.Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China;3.Chinese Pharmaceutical Association, Beijing 100022, China

Abstract:

OBJECTIVE To investigate the mechanism of doxorubicin-schisandrin B co-delivery liposomes(DSCL) to overcome multidrug resistance(MDR). METHODS DSCL were prepared. The K562/DOX cells were chosen as the model cells. The low temperature test, Endocytosis inhibitors (chloroquine, sodium azide, and mannitol) test were carried out on K562/DOX cells. And P-gp expression and apoptosis were detected by flow cytometry. RESULTS The uptake of DSCL was energy-dependent and was influenced by temperature, and endocytosis inhibitors, such as chloroquine, sodium azide and mannitol, could decrease significantly accumulation of DOX. The flow cytometry result revealed that the expression of P-gp of K562/DOX cells was significantly inhibited after treatment with DSCL, and it showed DSCL induced a regulated apoptotis in cells. CONCLUSION DSCL were uptaken through the endocytosis of energy-dependent. It is proposed the mechanism of DSCL to overcome multidrug resistance was a dual strategy by inhibiting the expression of P-gp and promoting apoptotis.

Key words: doxorubicin schisandrin B co-delivery liposomes multidrug resistance mechanism