Supplementation with Saccharomyces boulardii ameliorates hypoxia/reoxygenation-induced necrotizing enterocolitis in young mice
Supplementation with Saccharomyces boulardii ameliorates hypoxia/reoxygenation-induced necrotizing enterocolitis in young mice
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DOI：
10.1055/s-2003-43580
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发表时间：
2003-10-01
影响因子：
1.8
通讯作者：
Kultursay, N
中科院分区：
文献类型：
--
作者：
Akisu, M;Baka, M;Kultursay, N
肠道细菌增殖是新生儿坏死性小肠结肠炎（NEC）胃肠道损伤的一个重要方面。在本研究中，我们研究了口服补充布拉氏酵母菌（S. boulardii）（一种非病原体益生菌酵母）对年轻小鼠缺氧复氧（H/R）诱导的 NEC 的保护作用。年轻小鼠被分为三组；第 1 组小鼠（未治疗）仅接受缺氧-复氧；第2组小鼠接受缺氧-复氧，然后通过口胃插管每天两次给予冻干的布拉氏酵母菌（10mg悬浮于0.5ml盐水中），持续10天。第 3 组小鼠作为对照。将幼鼠放入 100% CO2 室中 5 分钟，诱导缺氧。缺氧后，幼鼠用100%氧气重新充氧10分钟。我们通过光学显微镜检查了肠道病变，并测量了 H/R 诱导的 NEC 模型中 PAF 和 TNF-α 的肠道生成。在益生菌组中，NEC 引起的肠道组织损伤大大减弱，坏死部分局限于粘膜。未治疗组的肠道组织 PAF 和 TNF-α 浓度均显着高于对照组 (p < 0.001)。与未治疗的幼鼠相比，补充布拉氏酵母菌的幼鼠肠道中 PAF 的生成量显着减少 (p < 0.05)。另一方面，未治疗组和益生菌组之间的肠道 TNF-α 浓度没有观察到显着差异 (p > 0.05)。本研究表明缺氧/复氧在 NEC 的发病机制中起着重要作用，并支持以下假设：尤其是 PAF 和 TNF-α 参与 H/R 诱导的 NEC 的病理生理机制。这项研究还表明，饮食中补充布拉氏酵母菌可改善 H/R 诱导的肠道损伤的组织学证据。基于这些发现，益生菌布拉氏酵母菌在这种 NEC 模型中的有益作用是通过抑制肠道促炎介质释放的机制介导的。
Intestinal bacterial proliferation is an important aspect of gastrointestinal injury in neonatal necrotizing enterocolitis (NEC). In the present investigation, we examined the protective action of oral supplementation with Saccharomyces boulardii (S. boulardii), non-pathogen probiotic yeast, against hypoxia-reoxygenation (H/R)-induced NEC in young mice. Young mice were divided into three groups; Group 1 mice (untreated) were subjected only to hypoxia-reoxygenation; Group 2 mice were subjected to hypoxia-reoxygenation and were then given Iyophilized S. boulardii (10 mg suspended in 0.5 ml saline) twice a day by orogastric intubation for 10 days. Group 3 mice served as controls. Hypoxia was induced by placing young mice in a 100% CO2 chamber for 5 min. After hypoxia, the young mice were reoxygenated for 10 min with 100% oxygen. We examined the intestinal lesions by light microscopy and measured intestinal generation of PAF and TNF-alpha in the H/R-induced model of NEC. In the probiotic group, NEC-induced intestinal tissue damage was greatly attenuated, with necrosis partially limited to the mucosa. Both intestinal tissue PAF and TNF-alpha concentrations were significantly higher in the untreated group than in controls (p < 0.001). S. boulardii-supplemented young mice showed a significant decrease in intestinal generation of PAF compared with untreated young mice (p < 0.05). On the other hand, no significant difference was observed in the intestinal concentration of TNF-alpha between untreated and probiotic groups (p > 0.05). The present study suggests that hypoxia/reoxygenation plays an important role in the pathogenesis of NEC and supports hypothesis that especially PAF and TNF-alpha are involved in the pathophysiological mechanism of H/R-induced NEC. This study also demonstrates that dietary supplementation with S. boulardii ameliorates the histologic evidence of H/R-induced intestinal injury. Based on these findings, the beneficial effects of probiotic S. boulardii in this model of NEC are mediated via mechanisms inhibiting intestinal proinflammatory mediator release.