中国体外循环杂志2025，Vol.23Issue(4)：354-360,7.DOI:10.13498/j.cnki.chin.j.ecc.2025.04.13
肠道菌群代谢产物丁酸减轻高氧诱导的小鼠肠损伤和中性粒细胞活化
Gut microbial metabolite butyrate alleviates hyperoxia-induced intestinal injury and neutrophil activation in mice
摘要
Abstract
Objective To investigate the effects of hyperoxia exposure on intestinal bacteria metabolite short-chain fatty acids(SCFAs)in mice using metabolomics and to further elucidate the regulatory effect of butyrate on hyperoxia-induced intestinal injury and neutrophil activation.Methods 12 male C57BL/6 mice were randomly divided into a hyperoxia group(n=6,80%O2)and a control group(n=6,room air),for 96 hours.Colonic contents were collected for targeted SCFA detection.In addition,further butyric acid intervention and hyperoxia experiments were performed.32 male C57BL/6 mice of the same strain were selected,weighed and randomly divided into 4 groups(n=8 each):saline control group,saline hyperoxia group,sodium butyrate control group and sodium butyrate hyperoxia group.The saline control group and the sodium butyrate control group were maintained in an oxygen tank with normoxic environment for 96 h.The saline hyperoxia group and the sodium butyrate hyperoxia group were exposed to hyperoxia(FiO2 80%)for 96 h.Mice in the sodium butyrate group received daily sodium butyrate gavage(5 000 mg/kg),and the control group received equivalent sterile saline.Gavage was administered early three days before the start of the experiment and continuously for four days after the start of the experiment.Intestinal histopathological injury,intestinal barrier damage,inflammatory reactivity,and neutrophil activation were detected.Results Hyperoxia significantly reduced colonic levels of the SCFAs acetate,propionate,butyrate,and hexanoate(all VIP>1,P<0.05).Butyrate supplementing alleviated hyperoxia-induced intestinal histopathological damage and cell apoptosis.It attenuated intestinal barrier damage and upregulated the expression of tight junction proteins ZO-1(P=0.015)and occludin(P=0.002).Butyrate reduced intestinal inflammation,decreasing levels of the pro-inflammatory cytokines TNF-α and IL-1β(both P<0.0001),while increasing the anti-inflammatory cytokine IL-10(P<0.0001).Furthermore,butyrate attenuated hyperoxia-induced intestinal neutrophil activation,evidenced by decreased MPO levels(P<0.0001),and down-regulated expression of neutrophil related cytokines CXCL-1,CCL-3 and IL-8(all P<0.0001).Conclusion Hyperoxia inhibits the metabolism of SCFA(especially butyric acid)in the gut microbiota of mice,and supplementing butyrate reduces hyperoxia-induced intestinal injury by regulating neutrophil activation.关键词
高氧/肠损伤/肠道代谢/短链脂肪酸/丁酸/中性粒细胞/小鼠Key words
Hyperoxia/Gut injury/Gut metabolome/Short chain fatty acids/Butyrate/Neutrophils/Mice引用本文复制引用
秦汉,林龙,伍航,何英,田仁斌,邢周雄..肠道菌群代谢产物丁酸减轻高氧诱导的小鼠肠损伤和中性粒细胞活化[J].中国体外循环杂志,2025,23(4):354-360,7.基金项目
国家自然科学基金(82160370) （82160370）
贵州省科技计划项目(黔科合支撑[2022]一般179) （黔科合支撑[2022]一般179）
贵州茅台医院基金(MTyk2022-12) （MTyk2022-12）
贵州省高等学校重点实验室建设项目(黔教技[2023]020) （黔教技[2023]020）
