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Potential of Inactivated Bifidobacterium Strain in Attenuating Benzo(A)Pyrene Exposure-Induced Damage in Colon Epithelial Cells In Vitro

机译:灭活双歧杆菌菌株在体外衰减苯并(A)芘暴露损伤的潜力

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Long-term exposure to benzo(a)pyrene (BaP) poses a serious genotoxic threat to human beings. This in vitro study investigated the potential of inactivated Bifidobacterium animalis subsp. lactis BI-04 in alleviating the damage caused by BaP in colon epithelial cells. A concentration of BaP higher than 50 μM strongly inhibited the growth of colon epithelial cells. The colon epithelial cells were treated with 50 μM BaP in the presence or absence of inactivated strain BI-04 (~5 × 10 8 CFU/mL). The BaP-induced apoptosis of the colon epithelial cells was retarded in the presence of B. lactis BI-04 through activation of the PI3K/ AKT signaling pathway, and p53 gene expression was decreased. The presence of the BI-04 strain reduced the intracellular oxidative stress and DNA damage incurred in the colon epithelial cells by BaP treatment due to the enhanced expression of antioxidant enzymes and metabolism-related enzymes (CYP1A1). The data from comet assay, qRT-PCR, and western blot analysis showed that the cytotoxic effects of BaP on colon epithelial cells were largely alleviated because the bifidobacterial strain could bind to this carcinogenic compound. The in vitro study highlights that the consumption of commercial probiotic strain BI-04 might be a promising strategy to mitigate BaP cytotoxicity.
机译:长期暴露于苯并(a)芘(BAP)对人类构成严重的遗传毒性威胁。这种体外研究研究了灭活双歧杆菌患者的潜力。乳酸BI-04减轻了在结肠上皮细胞中由弯曲引起的损伤。高于50μm的浓度强烈抑制结肠上皮细胞的生长。在存在或不存在灭活菌株Bi-04(〜5×10 8 CFU / mL)的情况下,用50μm壳体处理结肠上皮细胞。通过激活PI3K / AKT信号通路的激活,在B.乳酸BI-04的存在下延迟了结肠上皮细胞的BAP诱导的凋亡,并且降低了P53基因表达。由于抗氧化酶和代谢相关酶(CYP1A1)的增强,Bi-04应变的存在降低了通过壳体上皮细胞中的细胞内氧化应激和在结肠上皮细胞中产生的DNA损伤。来自COMET测定,QRT-PCR和Western印迹分析的数据表明,由于双歧杆菌菌株可以与该致癌化合物结合,因此大大缓解了BAP对结肠上皮细胞的细胞毒性作用。体外研究突出显示,商业益生菌菌株BI-04的消耗可能是减轻BAP细胞毒性的有希望的策略。

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