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壳聚糖纳米粒通过调节 ROS 介导的线粒体损伤和内质网应激诱导肝癌细胞的抗肿瘤作用。

Chitosan nanoparticles induced the antitumor effect in hepatocellular carcinoma cells by regulating ROS-mediated mitochondrial damage and endoplasmic reticulum stress.

机构信息

a School of Pharmacy , Jinzhou Medical University , Jinzhou , P. R. China.

b School of Veterinary Medicine , Jinzhou Medical University , Jinzhou , P. R. China.

出版信息

Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):747-756. doi: 10.1080/21691401.2019.1577876.

DOI:10.1080/21691401.2019.1577876
PMID:30873872
Abstract

In recent years, numerous studies have confirmed the role of chitosan nanoparticles (CS NPs) as a promising drug delivery carrier for improving the efficiency of anticancer drug in the treatment of cancer. However, the possible biological effects of CS NPs on tumour cells and underlying mechanisms are still unclear. Recently, reactive oxygen species (ROS)-mediated cell apoptosis has been implicated in the regulation of cell death. In this study, we found that CS NPs induced the massive generation of ROS and resulted in apoptosis of hepatocellular carcinoma cells (SMMC-7721) through activating the mitochondrial pathway and endoplasmic reticulum stress. These results suggest an important role of ROS in CS NPs-induced cancer cell death.

摘要

近年来,大量研究证实壳聚糖纳米粒子(CS NPs)作为一种有前途的药物输送载体,可提高抗癌药物在癌症治疗中的效率。然而,CS NPs 对肿瘤细胞的可能生物学效应及其潜在机制仍不清楚。最近,活性氧(ROS)介导的细胞凋亡被认为参与了细胞死亡的调控。在本研究中,我们发现 CS NPs 通过激活线粒体途径和内质网应激诱导大量 ROS 的产生,导致肝癌细胞(SMMC-7721)发生细胞凋亡。这些结果表明 ROS 在 CS NPs 诱导的癌细胞死亡中发挥重要作用。

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