Lin Martin Hsiu-Chu, Chang Li-Ching, Chung Chiu-Yen, Huang Wei-Chao, Lee Ming-Hsueh, Chen Kuo-Tai, Lai Ping-Shan, Yang Jen-Tsung
Department of Neurosurgery, Chang Gung Memorial Hospital, Chia-Yi Branch, Chia-Yi 61363, Taiwan.
Department of Chemistry, National Chung Hsing University, Taichung 402, Taiwan.
Pharmaceutics. 2021 Nov 5;13(11):1877. doi: 10.3390/pharmaceutics13111877.
Glioblastoma multiforme (GBM) is the most common malignant primary neoplasm of the adult central nervous system originating from glial cells. The prognosis of those affected by GBM has remained poor despite advances in surgery, chemotherapy, and radiotherapy. Photochemical internalization (PCI) is a release mechanism of endocytosed therapeutics into the cytoplasm, which relies on the membrane disruptive effect of light-activated photosensitizers. In this study, phototherapy by PCI was performed on a human GBM cell-line using the topoisomerase II inhibitor etoposide (Etop) and the photosensitizer protoporphyrin IX (PpIX) loaded in nanospheres (Ns) made from generation-5 polyamidoamine dendrimers (PAMAM(G5)). The resultant formulation, Etop/PpIX-PAMAM(G5) Ns, measured 217.4 ± 2.9 nm in diameter and 40.5 ± 1.3 mV in charge. Confocal microscopy demonstrated PpIX fluorescence within the endo-lysosomal compartment, and an almost twofold increase in cellular uptake compared to free PpIX by flow cytometry. Phototherapy with 3 min and 5 min light illumination resulted in a greater extent of synergism than with co-administered Etop and PpIX; notably, antagonism was observed without light illumination. Mechanistically, significant increases in oxidative stress and apoptosis were observed with Etop/PpIX-PAMAM(G5) Ns upon 5 min of light illumination in comparison to treatment with either of the agents alone. In conclusion, simultaneous delivery and endo-lysosomal co-localization of Etop and PpIX by PAMAM(G5) Ns leads to a synergistic effect by phototherapy; in addition, the finding of antagonism without light illumination can be advantageous in lowering the dark toxicity and improving photo-selectivity.
多形性胶质母细胞瘤(GBM)是成人中枢神经系统最常见的起源于神经胶质细胞的原发性恶性肿瘤。尽管在手术、化疗和放疗方面取得了进展,但GBM患者的预后仍然很差。光化学内化(PCI)是一种将内吞治疗剂释放到细胞质中的机制,它依赖于光激活光敏剂的膜破坏作用。在本研究中,使用拓扑异构酶II抑制剂依托泊苷(Etop)和负载在由第5代聚酰胺胺树枝状大分子(PAMAM(G5))制成的纳米球(Ns)中的光敏剂原卟啉IX(PpIX),对人GBM细胞系进行PCI光疗。所得制剂Etop/PpIX-PAMAM(G5) Ns的直径为217.4±2.9 nm,电荷为40.5±1.3 mV。共聚焦显微镜显示内溶酶体区室中有PpIX荧光,流式细胞术显示与游离PpIX相比,细胞摄取几乎增加了两倍。3分钟和5分钟光照的光疗比联合使用Etop和PpIX产生了更大程度的协同作用;值得注意的是,在没有光照的情况下观察到拮抗作用。从机制上讲,与单独使用任何一种药物相比,Etop/PpIX-PAMAM(G5) Ns在光照5分钟后氧化应激和细胞凋亡显著增加。总之,PAMAM(G5) Ns同时递送Etop和PpIX并使其在内溶酶体中共定位,通过光疗产生协同作用;此外,在没有光照的情况下发现拮抗作用有利于降低暗毒性并提高光选择性。