坏死性小肠结肠炎
氧化应激
粪便细菌疗法
粪便
医学
生物
内科学
微生物学
艰难梭菌
抗生素
作者
Xiaomei Li,Xiaowen Li,Qingjuan Shang,Zongwei Gao,Fa‐Bao Hao,Hongjie Guo,Chunbao Guo
标识
DOI:10.1016/j.freeradbiomed.2017.03.011
摘要
Fecal microbiota transplantation (FMT) has been used successfully to treat a variety of gastroenterological diseases. The alterations of microbiota in mouse models of necrotizing enterocolitis (NEC) as well as in patients suggested the possibility of treating NEC with FMT. Here we show that FMT caused an improvement in the histopathology and symptoms of NEC in WT mice, but not Grx1-/- mice. FMT eliminated O2•– production and promoted NO production in experimental NEC mice though the modulation of S-glutathionylation of eNOS (eNOS-SSG). FMT decreased the extent of TLR4-mediated proinflammatory signaling though TLR9 in the intestinal mucosa tissue. FMT also suppressed intestinal apoptosis and bacterial translocation across the intestinal barrier, which was accompanied by decreased inflammatory cytokine levels, altered bacterial microbiota, and regulated lymphocyte proportions. FMT is effective in a mouse model of NEC through the modulation of oxidative stress and reduced colon inflammation.
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