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Role of TLR4/NF-κB in Damage to Intestinal Mucosa Barrier Function and Bacterial Translocation in Rats Exposed to Hypoxia

机译：在大鼠损伤肠黏膜屏障功能和细菌移位TLR4 / NF-κB的作用低氧

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摘要

The role of Toll-like receptor 4 (TLR4)uclear factor-kappa-B (NF-κB) in intestinal mucosal barrier damage and bacterial translocation under hypoxic exposure is unclear. Here, we investigated their role using an acute hypobaric hypoxia model. Adult Sprague-Dawley rats were divided into control (C), hypoxia (H), hypoxia+NF-κB inhibitor pyrrolidinedithiocarbamic acid (PDTC) (100 mg. kg) (HP), hypoxia+0.5 mg/kg lipopolysaccharide (HPL), and hypoxia+PDTC+LPS (HPL) group. Except control group, other four groups were placed in a hypobaric chamber set at 7000 m. Samples were collected at 72 h after pressure reduction. Damage in ultrastructure of the intestinal tract was examined by transmission electron microscopy and bacterial translocation was detected by cultivation. Kinetic turbidimetric assay was used to measure the serum LPS.ELISA was performed to detect TNF-α and IL-6 serum concentrations. Fluorescent quantitative RT-PCR was used to measure TLR4 mRNA levels was measured using quantitative RT-PCR and protein of NF-κB p65 was measured by western blotting. Different degrees of intestinal mucosa damage were observed in groups H and HL. The damage was significantly alleviated after blockage of the TLR4/NF-κB signaling pathway. PDTC- treatment also reversed hyoxia- and LPS-induced bacterial translocation rate and increased serum levels of LPS, TNF-α, and IL-6. TLR4 mRNA levels and NF-κB p65 expression were consistent with the serum factor results. This study suggested that TLR4 and NF-κB expression increased in rat intestinal tissues after acute hypoxia exposure. PDTC-treatment reversed TLR4 and NF-κB upregulation and alleviated damage to the intestinal tract and bacterial translocation. Thus, the TLR4/NF-κB signaling pathway may be critical to the mechanism underlying hypoxia-induced damage to intestinal barrier function and bacterial translocation.
机译：Toll样受体4（TLR4）/核因子-κB（NF-κB）在低氧暴露下肠粘膜屏障损伤和细菌易位的作用尚不清楚。在这里，我们使用急性低压缺氧模型调查了它们的作用。将成年Sprague-Dawley大鼠分为对照组（C），低氧（H），低氧+NF-κB抑制剂吡咯烷二硫代氨基甲酸（PDTC）（100 mg.kg）（HP），低氧+0.5 mg / kg脂多糖（HPL），低氧+ PDTC + LPS（HPL）组。除对照组外，其他四组均置于7000 m的减压室中。减压后72小时收集样品。通过透射电子显微镜检查肠道超微结构的损伤，并通过培养检测细菌移位。动力学比浊法测定血清LPS。ELISA法检测血清TNF-α和IL-6的浓度。荧光定量RT-PCR用于测量TLR4 mRNA水平，定量RT-PCR，NF-κBp65蛋白通过蛋白质印迹法测量。 H和HL组观察到不同程度的肠粘膜损伤。阻断TLR4 /NF-κB信号通路后，损伤明显减轻。 PDTC处理还逆转了低氧和LPS诱导的细菌易位率，并增加了LPS，TNF-α和IL-6的血清水平。 TLR4 mRNA水平和NF-κBp65表达与血清因子结果一致。这项研究表明急性缺氧暴露后大鼠肠道组织中TLR4和NF-κB表达增加。 PDTC处理逆转了TLR4和NF-κB的上调，减轻了肠道损害和细菌移位。因此，TLR4 /NF-κB信号通路可能对缺氧诱导的肠屏障功能和细菌易位性损伤的机制至关重要。

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    Han Luo; Ping Guo; Qiquan Zhou;

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  • 年(卷),期 -1(7),10
  • 年度 -1
  • 页码 e46291
  • 总页数 9
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