DOX-PLGA Nanoparticles Effectively Suppressed the Expression of Pro-Inflammatory Cytokines TNF-a, IL-6, iNOS, and IL-1β in MCF-7 Breast Cancer Cell Line.

IF 1.6 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Reports of Biochemistry and Molecular Biology Pub Date : 2024-01-01 DOI:10.61186/rbmb.12.4.530
Rawan Hassan Al-Saeedi, Mohammad Khalaj-Kondori, Mohammad Ali Hosseinpour Feizi, Jafar Hajavi
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引用次数: 0

Abstract

Background: Inflammation contributes to cancer pathobiology through different mechanisms. Higher levels of pro-inflammatory cytokines can lead to hyperinflammation and promote cancer development and metastasis. For cancer treatment, Doxorubicin (DOX) can be encapsulated into the poly-lactic-glycolic acid (PLGA) nanoparticles. This study aimed to investigate the impact of doxorubicin-loaded PLGA nanoparticles (DOX-PLGA NP) on the expression of pro-inflammatory genes TNF-α, IL-6, iNOS, and IL-1β in the MCF-7 cells.

Methods: The DOX-PLGA NP was prepared by loading doxorubicin into PLGA and characterized using dynamic light scattering (DLS) and atomic force microscopy (AFM). The cytotoxic effect of the nanoparticles was determined by the MTT assay, and their impacts on the expression of pro-inflammatory genes were assessed by qRT-PCR.

Results: The encapsulation efficiency and loading capacity were 60±1.5 and 1.13±0.21 percent, respectively. The zeta potential and mean DOX-PLGA nanoparticle size were -18±0.550 mV and 172±55.6 nm, respectively. The 50% inhibitory concentration (IC50) of the DOX-PLGA NP on MCF-7 cell viability was 24.55 µg/mL after 72 hours of treatment. The qRT-PCR results revealed that the 20 µg/mL concentration of the DOX-PLGA NP significantly suppressed the expression of the pro-inflammatory genes TNF-α, IL-6, iNOS, and IL-1β compared to DOX alone (20 µg/mL). Additionally, the suppression effect of DOX-PLGA NP on the expression of these pro-inflammatory genes was dose-dependent.

Conclusions: These results show that DOX-PLGA NP efficiently suppressed the expression of pro-inflammatory genes. Furthermore, encapsulation of DOX into PLGA nanoparticles significantly improved the effectiveness of DOX in suppressing pro-inflammatory genes in MCF-7 breast cancer cells.

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DOX-PLGA 纳米粒子能有效抑制 MCF-7 乳腺癌细胞系中促炎细胞因子 TNF-a、IL-6、iNOS 和 IL-1β 的表达。
背景:炎症通过不同机制导致癌症病理生物学。较高水平的促炎细胞因子可导致过度炎症,促进癌症的发展和转移。多柔比星(Doxorubicin,DOX)可封装在聚乳酸-乙醇酸(Poly-lactic-glycolic acid,PLGA)纳米颗粒中用于癌症治疗。本研究旨在探讨负载多柔比星的 PLGA 纳米颗粒(DOX-PLGA NP)对 MCF-7 细胞中促炎基因 TNF-α、IL-6、iNOS 和 IL-1β 表达的影响:在 PLGA 中加入多柔比星制备了 DOX-PLGA NP,并使用动态光散射(DLS)和原子力显微镜(AFM)对其进行了表征。用 MTT 法测定纳米颗粒的细胞毒性效应,并用 qRT-PCR 法评估其对促炎基因表达的影响:结果:纳米颗粒的包封效率为 60±1.5%,负载能力为 1.13±0.21%。Zeta电位和DOX-PLGA纳米粒的平均粒径分别为-18±0.550 mV和172±55.6 nm。处理 72 小时后,DOX-PLGA NP 对 MCF-7 细胞活力的 50% 抑制浓度(IC50)为 24.55 µg/mL。qRT-PCR 结果显示,与单用 DOX(20 µg/mL)相比,20 µg/mL 浓度的 DOX-PLGA NP 能显著抑制促炎基因 TNF-α、IL-6、iNOS 和 IL-1β 的表达。此外,DOX-PLGA NP 对这些促炎基因表达的抑制作用呈剂量依赖性:这些结果表明,DOX-PLGA NP 能有效抑制促炎基因的表达。结论:这些结果表明,DOX-PLGA NP 能有效抑制促炎基因的表达,而且将 DOX 包封到 PLGA 纳米颗粒中能显著提高 DOX 抑制 MCF-7 乳腺癌细胞中促炎基因的效果。
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来源期刊
Reports of Biochemistry and Molecular Biology
Reports of Biochemistry and Molecular Biology BIOCHEMISTRY & MOLECULAR BIOLOGY-
CiteScore
2.80
自引率
23.50%
发文量
60
审稿时长
10 weeks
期刊介绍: The Reports of Biochemistry & Molecular Biology (RBMB) is the official journal of the Varastegan Institute for Medical Sciences and is dedicated to furthering international exchange of medical and biomedical science experience and opinion and a platform for worldwide dissemination. The RBMB is a medical journal that gives special emphasis to biochemical research and molecular biology studies. The Journal invites original and review articles, short communications, reports on experiments and clinical cases, and case reports containing new insights into any aspect of biochemistry and molecular biology that are not published or being considered for publication elsewhere. Publications are accepted in the form of reports of original research, brief communications, case reports, structured reviews, editorials, commentaries, views and perspectives, letters to authors, book reviews, resources, news, and event agenda.
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