Liang Gong-Wen, Lu Wan-Liang, Wu Jin-Wei, Zhao Ji-Hui, Hong Hai-Yan, Long Chuan, Li Ting, Zhang Yu-Teng, Zhang Hua, Wang Jian-Cheng, Zhang Xuan, Zhang Qiang
State Key Laboratory of Natural and Biomimetic Drugs and School of Pharmaceutical Sciences, Peking University, Beijing 100083, China.
Fundam Clin Pharmacol. 2008 Aug;22(4):429-37. doi: 10.1111/j.1472-8206.2008.00613.x.
The multi-drug resistance (MDR) could be caused by the over-expression of adenosine triphosphate binding cassette transporters such as p-glycoprotein, thereby resulting in the efflux of anti-cancer drugs from the cells. An anti-resistant stealthy liposomal vincristine plus quinacrine was defined in this study. Human chronic myelogenous leukemia K562 and MDR K562 cells were included for comparisons. Anti-tumor activity studies were performed on female BALB/c nude mice with MDR K562 cell xenografts. Results showed that quinacrine was effective in reversing the resistance in the MDR K562 cells, and enhanced the anti-tumor effect of vincristine in K562 cells. The caspase-9 and -3 activities in the MDR K562 and K562 cells were increased with the dose rise of quinacrine. In the MDR K562 cell xenografts in mice, the anti-resistant tumor effect of the stealthy liposomal vincristine plus quinacrine was evidently observed. The enhanced anti-tumor effects of vincristine by quinacrine in the resistant/non-resistant K562 cells could be because of the direct injury and the potentiating apoptotic effect of vincristine via activating the initiator caspase-9 and subsequently the effector caspase-3, and the long circulatory effect of stealthy liposomes. The stealthy liposomal encapsulation of vincristine plus quinacrine could be a potential therapeutic approach for resistant human leukemia.
多药耐药性(MDR)可能由三磷酸腺苷结合盒转运蛋白(如P-糖蛋白)的过度表达引起,从而导致抗癌药物从细胞中流出。本研究定义了一种抗耐药性的隐形脂质体长春新碱加奎纳克林。纳入人类慢性粒细胞白血病K562和多药耐药K562细胞进行比较。对携带多药耐药K562细胞异种移植瘤的雌性BALB/c裸鼠进行抗肿瘤活性研究。结果表明,奎纳克林可有效逆转多药耐药K562细胞的耐药性,并增强长春新碱对K562细胞的抗肿瘤作用。随着奎纳克林剂量的增加,多药耐药K562和K562细胞中的半胱天冬酶-9和-3活性升高。在小鼠多药耐药K562细胞异种移植瘤中,明显观察到隐形脂质体长春新碱加奎纳克林的抗耐药肿瘤作用。奎纳克林在耐药/非耐药K562细胞中增强长春新碱的抗肿瘤作用可能是由于长春新碱的直接损伤以及通过激活起始半胱天冬酶-9进而激活效应半胱天冬酶-3所产生的增强凋亡作用,以及隐形脂质体的长循环作用。长春新碱加奎纳克林的隐形脂质体包封可能是耐药性人类白血病的一种潜在治疗方法。