中文摘要：

背景：Faecalibacterium prausnitzii（Fp）是一种肠道共生菌，其数量减少是炎症性肠病（IBD）患者肠道菌群紊乱的重要特征之一。既往研究显示Fp上清液在实验性结肠炎中具有明显的抗炎效应。目的：探讨Fp上清液在实验性结肠炎中的抗炎效应是否与抑制TLR4／NF-κB信号通路激活有关。方法：24只C57BL／6小鼠随机分为正常对照组、结肠炎模型组和Fp上清治疗组。通过予小鼠连续5 d饮用3．5％葡聚糖硫酸钠（DSS）建立急性结肠炎模型，观察小鼠体质量和结肠组织病理学变化，分别以real-time PCR和免疫组化法检测结肠组织TLR4 mRNA和磷酸化NF-κB p65（p-NF-κB p65）表达，ELISA法检测血清肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、环氧合酶-2（COX-2）水平。结果：与正常对照组相比，结肠炎模型组小鼠体质量明显下降，结肠缩短，结肠组织病理学评分、TLR4 mRNA和p-NF-κB p65表达以及血清TNF-α、IL-6、COX-2水平均显著升高（P＜0．05）。Fp上清治疗组上述指标均较结肠炎模型组显著改善（P＜0．05），其中血清炎症因子水平与正常对照组相比无明显差异（P＞0．05）。结论：Fp上清液通过抑制TLR4／NF-κB信号通路激活及其下游炎症因子表达，在实验性结肠炎中发挥抗炎效应。

英文摘要：

Background：Faecalibacterium prausnitzii（Fp）is one of the commensal bacteria colonized in intestine,lowering of Fp is the key character of intestinal microbial dysbiosis in patients with inflammatory bowel disease （IBD ）. It has been demonstrated that the supernatant of Fp exerts an obvious anti-inflammatory effect in experimental colitis. Aims：To investigate whether the anti-inflammatory effect of Fp supernatant in experimental colitis is related to inhibition of TLR4/NF-κB pathway activation. Methods：Twenty-four C57BL/6 mice were randomly divided into the normal control group, colitis group and Fp supernatant-treated group. Acute colitis was induced by drinking 3. 5% dextran sulfate sodium （DSS） in tap water for five days. Weight loss and histopathological damage of colon tissue were observed;real-time PCR and immunohistochemistry were applied to determine the TLR4 mRNA and phosphorylated NF-κB p65 （p-NF-κB p65 ） expression in colon tissue. Serum levels of tumor necrosis factor-α（TNF-α）,interleukin-6 （IL-6）and cyclooxygenase-2 （COX-2）were detected by ELISA method. Results：Compared with normal control group,mice in colitis group showed a heavier weight loss and shortened colon length;the colonic histopathological score,TLR4 mRNA and p-NF-κB p65 expressions,together with the serum levels of TNF-α,IL-6 and COX-2 were significantly increased （P〈0. 05）. When treated with Fp supernatant,all the above-mentioned indicators were reversed with statistical significance （P〈0. 05）. No significant differences were found in serum inflammatory cytokines between Fp supernatant-treated group and normal control＆amp;nbsp;group （P〉0. 05）. Conclusions：The mechanism for Fp supernatant against experimental colitis is related to the inhibition of TLR4/NF-κB pathway activation and suppression of downstream inflammatory cytokines.