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壳聚糖纳米粒子负载蜂毒对癌细胞系潜在的线粒体 ROS 介导的损伤。

Potential mitochondrial ROS-mediated damage induced by chitosan nanoparticles bee venom-loaded on cancer cell lines.

机构信息

Center for Microbiology and Phage Therapy, Zewail City of Science and Technology, Giza 12578, Egypt.

Department of Zoology, Faculty of Science, Cairo University, Giza, Egypt.

出版信息

Int J Biol Macromol. 2024 Nov;279(Pt 4):135362. doi: 10.1016/j.ijbiomac.2024.135362. Epub 2024 Sep 6.

DOI:10.1016/j.ijbiomac.2024.135362
PMID:39245116
Abstract

Recently, numerous studies have confirmed the importance of chitosan nanoparticles (CNP) as a viable drug delivery carrier for increasing the efficacy of anticancer drugs in cancer treatment. It is a macromolecule and natural biopolymer compound, more stable and safer in use than metal nanoparticles. Bee venom (BV), a form of defense venom, has been shown to have anti-tumor, neuroprotective, anti-inflammatory, analgesic, and anti-infectivity properties. Moreover, the regulation of cell death has been linked to reactive oxygen species (ROS)-mediated cell apoptosis, which induces mitochondrial damage and ER stress through oxidative stress events. Therefore, this study aimed to illustrate the ROS-mediated effect on the cancer cells treatment with CNP-loaded BV (CNP-BV) and explained the adverse effects of ROS generation on Mitochondria and ER. We have found that the targeted CNP-BV were high in cytotoxicity against MCF-7 (IC 437.2 μg/mL) and HepG2 (IC 109.5 μg/mL) through the induction of massive generation of ROS, which in turn results in activating the mitochondrial cascade and ER stress. These results highlighted the role of ROS generation in inducing apoptosis in cancer cells.

摘要

最近,许多研究证实了壳聚糖纳米粒子(CNP)作为一种可行的药物输送载体的重要性,可提高癌症治疗中抗癌药物的疗效。它是一种高分子量和天然生物聚合物化合物,比金属纳米粒子更稳定、更安全。蜂毒(BV)是一种防御毒液,已被证明具有抗肿瘤、神经保护、抗炎、镇痛和抗感染特性。此外,细胞死亡的调节与活性氧(ROS)介导的细胞凋亡有关,ROS 介导的细胞凋亡通过氧化应激事件诱导线粒体损伤和内质网应激。因此,本研究旨在说明 ROS 介导的 CNP 负载 BV(CNP-BV)对癌细胞的影响,并解释 ROS 产生对 Mitochondria 和 ER 的不良影响。我们发现,通过大量产生 ROS,靶向 CNP-BV 对 MCF-7(IC 437.2μg/mL)和 HepG2(IC 109.5μg/mL)具有高细胞毒性,这反过来又导致线粒体级联和内质网应激的激活。这些结果强调了 ROS 产生在诱导癌细胞凋亡中的作用。

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