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中国精品科技期刊2020
高超,刘杰,赵传欣. 人参寡肽抗苯并芘诱发肺上皮细胞炎性损伤研究[J]. 华体会体育,2021,42(16):336−343. doi: 10.13386/j.issn1002-0306.2020100138.
引用本文: 高超,刘杰,赵传欣. 人参寡肽抗苯并芘诱发肺上皮细胞炎性损伤研究[J]. 华体会体育,2021,42(16):336−343. doi: 10.13386/j.issn1002-0306.2020100138.
GAO Chao, LIU Jie, ZHAO Chuanxin. Ginseng Oligopeptides against Benzopyrene-Induced Inflammatory Injury of Lung Epithelial Cells[J]. Science and Technology of Food Industry, 2021, 42(16): 336−343. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2020100138.
Citation: GAO Chao, LIU Jie, ZHAO Chuanxin. Ginseng Oligopeptides against Benzopyrene-Induced Inflammatory Injury of Lung Epithelial Cells[J]. Science and Technology of Food Industry, 2021, 42(16): 336−343. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2020100138.

人参寡肽抗苯并芘诱发肺上皮细胞炎性损伤研究

Ginseng Oligopeptides against Benzopyrene-Induced Inflammatory Injury of Lung Epithelial Cells

  • 摘要: 本研究从人参中提取获得人参寡肽,解析其氨基酸序列;利用CCK-8技术筛选保护人肺上皮II型(A549)细胞免受苯并芘(Benzopyrene,Bap)损伤效果最好的寡肽;流式细胞术检测人参寡肽-1(Renshen Oligopeptides-1,RSO-1)在10 μmol/L及50 μmol/L浓度下对浓度为10 nmol/L的Bap导致的A549细胞凋亡、线粒体膜电位降低和活性氧(Reactive Oxygen Species, ROS)含量增加的影响;蛋白免疫印迹验证10 nmol/L浓度的Bap对A549细胞芳香烃受体(Aromatic Hydrocarbon Receptor,AHR)、NF-κB与MAPK信号通路及AP-1因子的影响,并检测了RSO-1在10及50 μmol/L浓度下对Bap毒性的抑制作用。结果表明,10 nmol/L的Bap暴露诱发A549细胞氧化应激(与空白对照组相比具有显著性差异,P<0.05),激活芳香烃受体(Aromatic Hydrocarbon Receptor,AHR)和NF-κB信号通路并诱发细胞凋亡(与空白对照组相比具有显著性差异,P<0.05)。而浓度为10和50 μmol/L人参寡肽(Ginseng Oligopeptide,RSO,RSO-1~氨基酸序列-EGHGF)均可抑制Bap暴露导致的AP-1因子表达及芳香烃受体(AHR)和NF-κB的激活,从而抑制Bap暴露导致的细胞凋亡(与Bap组相比均具有显著性差异,P<0.05)。本研究对人参的应用及深层次开发提供理论依据。

     

    Abstract: In this study, ginseng oligopeptides were extracted from ginseng, and the amino acid sequence was analyzed. CCK-8 technology was used to screen the oligopeptides with the best effect on protecting human lung epithelial type II (A549) cells from benzopyrene (Bap) damage. Flow cytometry detection of ginseng oligopeptide-1 (Renshen Oligopeptides-1, RSO-1) at 10 and 50 μmol/L concentration of 10 nmol/L Bap-induced A549 cell apoptosis and mitochondrial membrane. The effect of potential decreased and reactive oxygen species (ROS) content increased. Western blotting verified that Bap at a concentration of 10 nmol/L affects the Aromatic Hydrocarbon Receptor (AHR), NF-κB and MAPK signaling pathways in A549 cells and the influence of AP-1 factor, and tested the inhibitory effect of RSO-1 on Bap toxicity at 10 and 50 μmol/L. The results showed that 10 nmol/L Bap exposure induced oxidative stress in A549 cells (significantly different from the blank control group, P<0.05), activated aromatic hydrocarbon receptor (AHR) and NF-κB signaling pathway and induce cell apoptosis (compared with the blank control group, there was a significant difference, P<0.05). The concentration of 10 and 50 μmol/L ginseng oligopeptide (Ginseng Oligopeptide, RSO, RSO-1~amino acid sequence-EGHGF) could inhibit the expression of AP-1 factor and aryl hydrocarbon receptor (AHR) caused by Bap exposure and NF-κB activation, thereby inhibiting cell apoptosis was caused by Bap exposure (compared with Bap group, both have significant difference, P<0.05). This research would provide a theoretical basis for the application and in-depth development of ginseng.

     

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