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经昆虫肽 CopA3 处理后,可最大程度地降低黄曲霉毒素 B1 污染引起的炎症反应和相关风险,并对健康产生有益影响。

The inflammation response and risk associated with aflatoxin B1 contamination was minimized by insect peptide CopA3 treatment and act towards the beneficial health outcomes.

机构信息

Department of Biotechnology, Daegu University, Jillyang, Naeri-riGyeongsan, Gyeongbuk, 38453, Republic of Korea.

出版信息

Environ Pollut. 2021 Jan 1;268(Pt B):115713. doi: 10.1016/j.envpol.2020.115713. Epub 2020 Oct 5.

DOI:10.1016/j.envpol.2020.115713
PMID:33038573
Abstract

This study focused on the possible chemo-preventive effects of insect peptide CopA3 on normal human colon cells against the inflammation induced by the toxic environmental pollutant aflatoxin B1 (AFB1). In the study, we used CCD 841 CoN normal human colon cells to investigate the cytotoxic effect induced by AFB1 and elucidated the negative impact of AFB1 exposure on the cell cycle progression. Further, we also carried out the in-vivo experiment, where male BALB/c mice were administrated with AFB1 to induce inflammation associated cancer like phenotype and the dietary effect of CopA3 was evaluated on the early stages of AFB1-induced hepatotoxicity and inflammation in colon tissues. At the initiation stage, CopA3 was given along with water, which significantly decreased the inflammation in the liver and colon of AFB1 exposed mice model. Mice that received CopA3 alone showed enhanced activity of several antioxidant enzymes. In the post treatment stage, the CopA3 dosage remarkably increased the Ki-67 protein expression, indicating the enhancement in cell proliferation event and increased the number of apoptotic cells in colonic crypts, suggesting the capability of CopA3 treatment towards the epithelial cell turnover. Thus, CopA3 treatment shows its potential to inhibit the development of the early stages of AFB1-induced colon inflammation and hepatotoxicity in mice by inhibiting the DNA synthesis of the damaged and inflammatory cell and induced apoptosis for the clearance of damaged cells. Collectively, the results of this study suggest that CopA3 treatment may play a protective role against the mycotoxin induced inflammation.

摘要

本研究旨在探讨昆虫肽 CopA3 对正常人类结肠细胞的化学预防作用,以防止有毒环境污染物黄曲霉毒素 B1(AFB1)引起的炎症。在研究中,我们使用 CCD 841 CoN 正常人类结肠细胞来研究 AFB1 诱导的细胞毒性作用,并阐明 AFB1 暴露对细胞周期进程的负面影响。此外,我们还进行了体内实验,用 AFB1 处理雄性 BALB/c 小鼠以诱导与炎症相关的癌症样表型,并评估 CopA3 在 AFB1 诱导的肝毒性和结肠组织炎症的早期阶段的饮食效应。在起始阶段,CopA3 与水一起给予,这显著降低了 AFB1 暴露小鼠模型中肝脏和结肠的炎症。单独接受 CopA3 的小鼠表现出几种抗氧化酶活性增强。在治疗后期,CopA3 剂量显著增加了 Ki-67 蛋白表达,表明细胞增殖事件增强,并增加了结肠隐窝中凋亡细胞的数量,表明 CopA3 治疗对上皮细胞更新的能力。因此,CopA3 治疗通过抑制受损和炎症细胞的 DNA 合成以及诱导凋亡以清除受损细胞,显示出抑制 AFB1 诱导的结肠炎症和肝毒性早期发展的潜力。总之,这项研究的结果表明,CopA3 治疗可能在对抗真菌毒素诱导的炎症中发挥保护作用。

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