Sine Jessica, Urban Cordula, Thayer Derek, Charron Heather, Valim Niksa, Tata Darrell B, Schiff Rachel, Blumenthal Robert, Joshi Amit, Puri Anu
Membrane Structure and Function Section, Basic Research Laboratory, Center for Cancer Research, National Cancer Institute - Frederick, Frederick, MD, USA.
Department of Radiology, Baylor College of Medicine, Houston, TX, USA.
Int J Nanomedicine. 2014 Dec 19;10:125-45. doi: 10.2147/IJN.S72143. eCollection 2015.
We recently reported laser-triggered release of photosensitive compounds from liposomes containing dipalmitoylphosphatidylcholine (DPPC) and 1,2 bis(tricosa-10,12-diynoyl)-sn-glycero-3-phosphocholine (DC(8,9)PC). We hypothesized that the permeation of photoactivated compounds occurs through domains of enhanced fluidity in the liposome membrane and have thus called them "Pocket" liposomes. In this study we have encapsulated the red light activatable anticancer photodynamic therapy drug 2-(1-Hexyloxyethyl)-2-devinyl pyropheophorbide-a (HPPH) (Ex/Em410/670 nm) together with calcein (Ex/Em490/517 nm) as a marker for drug release in Pocket liposomes. A mole ratio of 7.6:1 lipid:HPPH was found to be optimal, with >80% of HPPH being included in the liposomes. Exposure of liposomes with a cw-diode 660 nm laser (90 mW, 0-5 minutes) resulted in calcein release only when HPPH was included in the liposomes. Further analysis of the quenching ratios of liposome-entrapped calcein in the laser treated samples indicated that the laser-triggered release occurred via the graded mechanism. In vitro studies with MDA-MB-231-LM2 breast cancer cell line showed significant cell killing upon treatment of cell-liposome suspensions with the laser. To assess in vivo efficacy, we implanted MDA-MB-231-LM2 cells containing the luciferase gene along the mammary fat pads on the ribcage of mice. For biodistribution experiments, trace amounts of a near infrared lipid probe DiR (Ex/Em745/840 nm) were included in the liposomes. Liposomes were injected intravenously and laser treatments (90 mW, 0.9 cm diameter, for an exposure duration ranging from 5-8 minutes) were done 4 hours postinjection (only one tumor per mouse was treated, keeping the second flank tumor as control). Calcein release occurred as indicated by an increase in calcein fluorescence from laser treated tumors only. The animals were observed for up to 15 days postinjection and tumor volume and luciferase expression was measured. A significant decrease in luciferase expression and reduction in tumor volume was observed only in laser treated animal groups injected with liposomes containing HPPH. Histopathological examination of tumor tissues indicated tumor necrosis resulting from laser treatment of the HPPH-encapsulated liposomes that were taken up into the tumor area.
我们最近报道了从含有二棕榈酰磷脂酰胆碱(DPPC)和1,2-双(二十三碳-10,12-二炔酰基)-sn-甘油-3-磷酸胆碱(DC(8,9)PC)的脂质体中激光触发释放光敏化合物。我们推测光活化化合物的渗透是通过脂质体膜中流动性增强的区域发生的,因此将它们称为“口袋”脂质体。在本研究中,我们将红光可激活的抗癌光动力治疗药物2-(1-己氧基乙基)-2-去乙烯基焦脱镁叶绿酸-a(HPPH)(激发/发射波长410/670nm)与钙黄绿素(激发/发射波长490/517nm)一起封装在口袋脂质体中,作为药物释放的标记物。发现脂质与HPPH的摩尔比为7.6:1是最佳的,超过80%的HPPH被包封在脂质体中。用连续波二极管660nm激光(90mW,0 - 5分钟)照射脂质体,只有当脂质体中包含HPPH时才会导致钙黄绿素释放。对激光处理样品中脂质体包裹的钙黄绿素的猝灭率进行进一步分析表明,激光触发释放是通过分级机制发生的。对MDA-MB-231-LM2乳腺癌细胞系进行的体外研究表明,用激光处理细胞-脂质体悬浮液后有显著的细胞杀伤作用。为了评估体内疗效,我们将含有荧光素酶基因的MDA-MB-231-LM2细胞植入小鼠胸腔的乳腺脂肪垫中。对于生物分布实验,脂质体中包含微量的近红外脂质探针DiR(激发/发射波长745/840nm)。静脉注射脂质体,并在注射后4小时进行激光治疗(90mW,直径0.9cm,暴露持续时间5 - 8分钟)(每只小鼠仅治疗一个肿瘤,将另一侧胁腹肿瘤作为对照)。仅激光处理的肿瘤中钙黄绿素荧光增加表明发生了钙黄绿素释放。在注射后长达15天观察动物,并测量肿瘤体积和荧光素酶表达。仅在注射含有HPPH的脂质体的激光治疗动物组中观察到荧光素酶表达显著降低和肿瘤体积减小。对肿瘤组织的组织病理学检查表明,激光处理摄取到肿瘤区域的包封HPPH的脂质体导致了肿瘤坏死。