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乳酸菌对铁诱导的小鼠结肠氧化应激的抑制作用。

Inhibition of Fe-induced colon oxidative stress by lactobacilli in mice.

机构信息

School of Food Science and Technology, Jiangnan University, Wuxi 214122, Jiangsu Province, China.

出版信息

World J Microbiol Biotechnol. 2013 Feb;29(2):209-16. doi: 10.1007/s11274-012-1172-5. Epub 2012 Sep 19.

Abstract

Iron (Fe) can promote hydrogen peroxide (H(2)O(2)) and hydroxyl radical generation in the colonic surface and promote growth of Fe-dependent bacteria. Some Lactobacillus strains are resistant to oxygen free-radicals, allowing them to survive in a Fe-modulated mucosal environment and influence colon microbial ecology and redox state. Here, we investigated the capacity of lactobacilli with different antioxidant abilities to modify the bacterial profile and prevent oxidative stress in the colon of Fe-overloaded mice. Survival time of Lactobacillus rhamnosus LGG (LGG) in the presence of H(2)O(2) and hydroxyl radical was significantly longer compared with the mid- and non-antioxidative strains, Lactobacillus paracasei Fn032 and Lactobacillus plantarum Fn001, respectively. Different Lactobacillus strains are specific in free-radical scavenging activities of their cell-free extracts, which increased to varying extent depending on strains when bacteria were exposed to simulated gastric and pancreatic juice. Fe-overloaded mice showed increased colonic luminal ferrous Fe content, Enterococcus and Escherichia coli concentrations, mucosal malondialdehyde and free-radicals, and decreased mucosal total antioxidative capacity and oxidative enzymatic activity. Translocation of endotoxin to the liver was also significantly increased (P < 0.05). Lactobacilli inhibited ferrous Fe accumulation, especially in LGG and Fn032. LGG significantly inhibited the increase of colonic mucosal free-radicals and malondialdehyde content (P < 0.05). Fn032 only inhibited malondialdehyde (P < 0.05). LGG and Fn032 significantly inhibited increases in colonic Enterococcus (P < 0.05). Fn001 showed no significant antioxidative ability in vivo. The difference of these effects in vivo were well agreed with scavenging activities against reactive oxygen species (ROS) of simulated gastrointestinals fluid pretreated cells in vitro. In conclusion, ROS scavenging activities was essential for Lactobacillus to prevent oxidative stress in vivo and inhibition of ROS-producing bacterial growth and mucosal barrier injury.

摘要

铁(Fe)可以促进结肠表面过氧化氢(H 2 O 2 )和羟自由基的生成,并促进 Fe 依赖性细菌的生长。一些乳杆菌菌株对氧自由基有抵抗力,使它们能够在 Fe 调节的粘膜环境中存活,并影响结肠微生物生态和氧化还原状态。在这里,我们研究了具有不同抗氧化能力的乳杆菌菌株改变细菌谱并防止 Fe 过载小鼠结肠氧化应激的能力。与中抗氧化和非抗氧化菌株,即副干酪乳杆菌 Fn032 和植物乳杆菌 Fn001 相比,鼠李糖乳杆菌 LGG(LGG)在存在 H 2 O 2 和羟自由基的情况下的存活时间明显更长。不同的乳杆菌菌株对其无细胞提取物的自由基清除活性具有特异性,当细菌暴露于模拟胃液和胰液时,根据菌株的不同,其活性会不同程度地增加。Fe 过载小鼠显示出增加的结肠腔铁含量、肠球菌和大肠杆菌浓度、粘膜丙二醛和自由基,以及降低的粘膜总抗氧化能力和氧化酶活性。内毒素向肝脏的易位也显著增加(P < 0.05)。乳杆菌抑制亚铁 Fe 的积累,特别是在 LGG 和 Fn032 中。LGG 显著抑制结肠粘膜自由基和丙二醛含量的增加(P < 0.05)。Fn032 仅抑制丙二醛(P < 0.05)。LGG 和 Fn032 显著抑制结肠肠球菌的增加(P < 0.05)。Fn001 体内没有显示出明显的抗氧化能力。这些体内作用的差异与体外模拟胃肠液预处理细胞对活性氧(ROS)的清除活性非常一致。总之,ROS 清除活性对于乳杆菌预防体内氧化应激以及抑制 ROS 产生细菌的生长和粘膜屏障损伤是必不可少的。

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