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Chitosan nanoparticles loaded with aspirin and 5-fluororacil enable synergistic antitumour activity through the modulation of NF-κB/COX-2 signalling pathway.
IET Nanobiotechnology ( IF 3.8 ) Pub Date : 2020-08-06 , DOI: 10.1049/iet-nbt.2020.0002
Peng Wang 1 , Yaping Shen 2 , Liang Zhao 2
Affiliation  

Based on the enhancement of synergistic antitumour activity to treat cancer and the correlation between inflammation and carcinogenesis, the authors designed chitosan nanoparticles for co-delivery of 5-fluororacil (5-Fu: an as anti-cancer drug) and aspirin (a non-steroidal anti-inflammatory drug) and induced synergistic antitumour activity through the modulation of the nuclear factor kappa B (NF-κB)/cyclooxygenase-2 (COX-2) signalling pathways. The results showed that aspirin at non-cytotoxic concentrations synergistically sensitised hepatocellular carcinoma cells to 5-Fu in vitro. It demonstrated that aspirin inhibited NF-κB activation and suppressed NF-κB regulated COX-2 expression and prostaglandin E2 (PGE2) synthesis. Furthermore, the proposed results clearly indicated that the combination of 5-Fu and aspirin by chitosan nanoparticles enhanced the intracellular concentration of drugs and exerted synergistic growth inhibition and apoptosis induction on hepatocellular carcinoma cells by suppressing NF-κB activation and inhibition of expression of COX-2.

中文翻译:

负载阿司匹林和 5-氟嘧啶的壳聚糖纳米颗粒通过调节 NF-κB/COX-2 信号通路实现协同抗肿瘤活性。

基于增强治疗癌症的协同抗肿瘤活性以及炎症与致癌之间的相关性,作者设计了壳聚糖纳米粒,用于共同递送 5-氟嘧啶(5-Fu:一种抗癌药物)和阿司匹林(一种非甾体抗炎药)并通过调节核因子κB(NF-κB)/环氧合酶2(COX-2)信号通路诱导协同抗肿瘤活性。结果表明,非细胞毒性浓度的阿司匹林在体外协同增敏肝细胞癌细胞对 5-Fu 的敏感性。它表明阿司匹林抑制 NF-κB 活化并抑制 NF-κB 调节 COX-2 表达和前列腺素 E2 (PGE2) 合成。此外,
更新日期:2020-08-20
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