罗伊氏乳杆菌对坏死性小肠结肠炎氧化应激的保护机制 |
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引用本文: | 唐佳,郭春宝,龚放.罗伊氏乳杆菌对坏死性小肠结肠炎氧化应激的保护机制[J].南方医科大学学报,2019,39(10):1221. |
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作者姓名: | 唐佳 郭春宝 龚放 |
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作者单位: | 重庆医科大学附属永川医院新生儿科,重庆,402160;重庆医科大学附属儿童医院肝胆外科,重庆,400014 |
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基金项目: | 国家自然科学基金;国家自然科学基金;国家自然科学基金;重庆市自然科学基金重点项目;重庆市自然科学基金重点项目;重庆市自然科学基金重点项目 |
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摘 要: | 目的探讨罗伊氏乳杆菌(L. reuteri)DSM17938菌株对坏死性小肠结肠炎(NEC)新生小鼠模型氧化应激的保护作用及可
能机制。方法将96只10日龄C57BL/6J新生小鼠随机分为3组(n=32):对照组、NEC组、NEC+L. reuteri组。通过HE染色观察
回盲部肠组织病理变化并行双盲病理评分。采用实时荧光定量PCR检测肠组织中TNF-α、IL-1β的基因表达水平。通过ELISA
检测肠组织TNF-α、IL-1β的蛋白表达水平。采用比色法检测SOD活力及抑制率、MDA、GSH、GSSG、GSSG/GSH比值。结果
与对照组相比,NEC组小鼠体质量下降(P<0.05),肠道损伤加重,病理评分增加(P<0.05),TNF-α、IL-1β在基因及蛋白水平均表
达升高(P<0.05),SOD活力及抑制率、GSH降低,MDA、GSSG、GSSG/GSH比值显著升高(P<0.05)。与NEC组相比,NEC+L.
reuteri 组病理评分降低,TNF-α、IL-1β在基因及蛋白水平均表达降低(P<0.05),SOD活力及抑制率、GSH 增加,MDA、GSSG、
GSSG/GSH比值明显降低(P<0.05),两组生存率差异无统计学意义(P>0.05)。结论L. reuteri DSM17938可能通过减少肠道
氧化应激、增加其抗氧化能力,从而减轻肠道炎症反应,发挥对NEC新生小鼠肠道保护作用。
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关 键 词: | 罗伊氏乳杆菌DSM17938 坏死性小肠结肠炎 炎症因子 氧化应激 |
Protective effect of Lactobacillus reuteri against oxidative stress in neonatal mice with
necrotizing enterocolitis |
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Abstract: | Objective To investigate the protective effect of L. reuteri DSM17938 strain against oxidative stress in a neonatal
mouse model of necrotizing enterocolitis (NEC) and explore the possible mechanism. Methods Ninety-six 10-day-old neonatal
C57BL/6J mice were equally randomized into control group, NEC group, and NEC+ L. reuteri group. The pathological changes
of the ileocecal intestinal tissue were evaluated with HE staining and double-blind pathological scoring. The mRNA and
protein expressions of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the intestinal tissues were detected using
quantitative real-time PCR and ELISA, respectively. Colorimetric assays were used to determine the activity of superoxide
dismutase (SOD) and its inhibition rate, malondialdehyde (MDA), glutathione (GSH), oxidized glutathione (GSSG), and GSSG/
GSH ratio. Results Compared with those in the control group, the neonatal mice in NEC group showed significant weight loss
(P<0.05), obvious intestinal injury, increased pathological scores (P<0.05), increased expressions of TNF-α and IL-1β mRNA
and proteins (P<0.05), decreased SOD activity and inhibition rate, decreased GSH, and significantly increased MDA, GSSG,
and GSSG/GSH ratios (P<0.05). Treatment with L. reuteri obviously decreased the pathological scores, expressions of TNF-α
and IL-1β (P<0.05), MDA, GSSG, and GSSG/GSH ratio (P<0.05), and significantly increased SOD activity, its inhibition rate, and
GSH level in the mice with NEC, but the survival rate was not significantly different between NEC and L. reuteri-treated
groups (P>0.05). Conclusion L. reuteri DSM17938 can offer protection against NEC in mice by reducing oxidative stress and
increasing antioxidant capacity of the intestinal tissue to suppress intestinal inflammations. |
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