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Apple polysaccharide prevents from colitis-associated carcinogenesis through regulating macrophage polarization.

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机构: [1]Key Laboratory of Gastrointestinal Pharmacology of Chinese Materia Medica of the State Administration of Traditional Chinese Medicine, Department of Pharmacology, School of Pharmacy, the Fourth Military Medical University, Xi’an 710032, Shaanxi, PR China [2]Department of Cardiology, Changhai Hospital, Naval Military Medical University, Shanghai 200433, PR China [3]Key Laboratory for Space Bioscience and Biotechnology, School of Life Sciences, Northwestern Polytechnical University, Xi’an 710072, Shaanxi, PR China [4]Department of Pharmacy, the First Naval Force Hospital of Southern Theatre Command, Zhanjiang 524005, Guangdong, PR China [5]Department of Microbial and Biochemical Pharmacy, School of Pharmacy, Southwest Medial University, Luzhou, 646000, Sichuan, PR China
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关键词: Apple polysaccharide Toll-like receptor 4 Macrophage polarization AOM Azoxymethane AP Apple polysaccharide CACC Colitis associated colorectal cancer CRC Colorectal cancer DSS Dextran sodium sulfate IME Inflammatory microenvironment TAM Tumor-associated macrophages TME Tumor microenvironment UC Ulcerative colitis

摘要:
Macrophages, an important component of inflammatory microenvironment and tumor microenvironment, are closely related to tumor development and progression. Our previous studies showed that apple polysaccharide (AP) could prevent from colitis associated colorectal carcinogenesis. Herein, we further our study to observe the effect of AP on the polarization of macrophages in Raw 264.7 cells and a colitis associated colorectal cancer mouse model, and to investigate the possible mechanisms. Forty male ICR mice were administered with azoxymethane (AOM) and dextran sodium sulfate (DSS). Twenty mice were given no further treatment as model mice, the rest twenty were fed basal diet mixed with 5% of AP. Raw 264.7 cells were treated with 0.5 mg/mL AP. AP could protect ICR mice against AOM/DSS-induced carcinogenesis, keep the colon of AOM/DSS-treated mice in a moderative inflammatory state, and shift macrophage polarization toward M1 phenotype. In vitro study showed that AP could upregulate TLR-4 signaling mildly and trigger M1 macrophage transition. Moreover, AP-induced transition of macrophage phenotype was suppressed by a TLR-4 antagonist, TAK-242. These data may provide a novel molecular basis for understanding how apples act to prevent colorectal cancer (CRC) and indicate that AP has a potential to prevent and treat CRC. Copyright © 2020 Elsevier B.V. All rights reserved.

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出版当年[2019]版:
大类 | 2 区 化学
小类 | 2 区 应用化学 2 区 高分子科学 3 区 生化与分子生物学
最新[2025]版:
大类 | 2 区 生物学
小类 | 2 区 生化与分子生物学 2 区 应用化学 2 区 高分子科学
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出版当年[2018]版:
Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Q1 POLYMER SCIENCE Q1 CHEMISTRY, APPLIED
最新[2023]版:
Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Q1 CHEMISTRY, APPLIED Q1 POLYMER SCIENCE

影响因子: 最新[2023版] 最新五年平均 出版当年[2018版] 出版当年五年平均 出版前一年[2017版] 出版后一年[2019版]

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第一作者机构: [1]Key Laboratory of Gastrointestinal Pharmacology of Chinese Materia Medica of the State Administration of Traditional Chinese Medicine, Department of Pharmacology, School of Pharmacy, the Fourth Military Medical University, Xi’an 710032, Shaanxi, PR China
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通讯机构: [4]Department of Pharmacy, the First Naval Force Hospital of Southern Theatre Command, Zhanjiang 524005, Guangdong, PR China [5]Department of Microbial and Biochemical Pharmacy, School of Pharmacy, Southwest Medial University, Luzhou, 646000, Sichuan, PR China [*1]Department of Pharmacy, the First Naval Force Hospital of Southern Theatre Command, Zhanjiang 524005, Guangdong, PR China [*2]Department of Microbial and Biochemical Pharmacy, School of Pharmacy, Southwest Medical University, Luzhou, 646000, Sichuan, PR China.
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