虾青素对氧化应激的保护作用:减轻 TNF-α 诱导的 SW480 细胞氧化损伤和氮氧甲烷/硫酸葡聚糖钠诱发的 C57BL/6 小鼠结肠炎相关癌症。

IF 4.9 2区 医学 Q1 CHEMISTRY, MEDICINAL
Marine Drugs Pub Date : 2024-10-12 DOI:10.3390/md22100469
Haifeng Zhang, Min Wang, Yu Zhou, Shaojie Bao, Feng Wang, Chunmei Li
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引用次数: 0

摘要

本研究探讨了虾青素(AST)对偶氮甲烷(AOM)和葡聚糖硫酸钠(DSS)联合诱导的结肠炎相关癌(CAC)和TNF-α诱导的人大肠癌细胞(SW480)氧化应激的保护作用及其内在机制。体外实验显示,虾青素可减少活性氧(ROS)的产生,抑制磷酸化JNK(P-JNK)、磷酸化ERK(P-ERK)、磷酸化p65(P-p65)和NF-κB下游蛋白环氧化酶-2(COX-2)的表达。体内实验表明,虾青素可改善 AOM/DSS 引起的体重减轻、结肠长度缩短和组织形态变化。此外,虾青素通过调节 MAPK 和 NF-κB 通路,抑制促炎细胞因子 IL-6、IL-1β 和 TNF-α 的表达,从而抑制细胞炎症。总之,虾青素可通过其抗氧化作用减轻细胞炎症和CAC。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Protective Effects of Astaxanthin against Oxidative Stress: Attenuation of TNF-α-Induced Oxidative Damage in SW480 Cells and Azoxymethane/Dextran Sulfate Sodium-Induced Colitis-Associated Cancer in C57BL/6 Mice.

In this study, we investigated the protective effects of astaxanthin (AST) against oxidative stress induced by the combination of azoxymethane (AOM) and dextran sulfate sodium (DSS) in colitis-associated cancer (CAC) and TNF-α-induced human colorectal cancer cells (SW480), as well as the underlying mechanism. In vitro experiments revealed that astaxanthin reduced reactive oxygen species (ROS) generation and inhibited the expression of Phosphorylated JNK (P-JNK), Phosphorylated ERK (P-ERK), Phosphorylated p65 (P-p65), and the NF-κB downstream protein cyclooxygenase-2 (COX-2). In vivo experiments showed that astaxanthin ameliorated AOM/DSS-induced weight loss, shortened the colon length, and caused histomorphological changes. In addition, astaxanthin suppressed cellular inflammation by modulating the MAPK and NF-κB pathways and inhibiting the expression of the proinflammatory cytokines IL-6, IL-1β, and TNF-α. In conclusion, astaxanthin attenuates cellular inflammation and CAC through its antioxidant effects.

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来源期刊
Marine Drugs
Marine Drugs 医学-医药化学
CiteScore
9.60
自引率
14.80%
发文量
671
审稿时长
1 months
期刊介绍: Marine Drugs (ISSN 1660-3397) publishes reviews, regular research papers and short notes on the research, development and production of drugs from the sea. Our aim is to encourage scientists to publish their experimental and theoretical research in as much detail as possible, particularly synthetic procedures and characterization information for bioactive compounds. There is no restriction on the length of the experimental section.
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