细菌脂多糖免疫对结肠炎小鼠TNF-α表达的影响.doc.docVIP

细菌脂多糖免疫对结肠炎小鼠TNF-α表达的影响 [摘要]目的：为了研究细菌脂多糖免疫对结肠炎小鼠TNF-α表达的影响并探讨炎症性肠炎的发生机制。方法：设计动物模型实验，将30只BALB/C小鼠随机分为三组：观察组10只（注射细菌脂多糖免疫后诱导小鼠溃疡性结肠炎模型）、模型组10只（注射生理盐水后诱导小鼠溃疡性结肠炎模型）和对照组10只（不做任何处理并注射生理盐水），4周后处死并取结肠组织标本检测，统计炎症介质TNF-α的表达情况并进行比较。结果：观察组血清TNF-αmRNA含量均值为（16.36±1.28）%，结肠TNF-α含量均值为（23.25±2.15）%，数据结果与其他两组差异具有统计学意义（P0.05）。结论：细菌脂多糖可降低小鼠结肠粘膜TNF-α及血清TNF-α的含量，这可能为其对溃疡性结肠炎的治疗提供理论依据。 [关键词]细菌脂多糖；溃疡性结肠炎；肿瘤坏死因子 Effect of LSP on the expression of TNF- α immunity in mice with colitis [Abstract] Objective: To study the influence of LSP on the expression of TNF- α immunological colitis in mice and to explore the mechanisms of IBD. Methods: the experiment animal model design, 30 male BALB/C mice were randomly divided into three groups: the observation group 10 (IBD models were induced by injection of LSP after immunization), 10 rats in model group (IBD mice models were induced by injection of saline) and 10 in control group (without any treatment and injection of physiological saline), 4 weeks after the colon tissue samples were taken for detection, and compared the expression of inflammatory mediators in TNF- α statistics. Results: in the observation group, serum TNF- α mRNA content was (16.36 ± 1.28)%, the mean content of TNF- α colon was (23.25 ± 2.15)%, with statistical significance of data and other differences between the two groups (P0.05). Conclusion: LSP can reduce the content of the colon mucosa of TNF- α and serum TNF- α, which may provide the theoretical basis for the treatment [Keywords]LSP; IBD; tumor necrosis factor 炎症性肠病（inflammatory bowel disease,IBD）是一类由多种不明病因引起的、异常免疫介导的肠道慢性及复发性炎症，有终身复发倾向，主要疾病类型有溃疡性结肠炎（ulcerative colitis,UC）和克罗恩病（Crohn disease,CD）。目前病因不明确，有学者认为环境、遗传、微生物感染和肠壁黏膜免疫异常，肠道黏膜损失等因素共同作用于IBD的发作[1]。以ELISA法检测IBD及其他胃肠道疾病患者抗结肠抗体时发现，溃疡性结肠炎患者抗结肠抗体出现率为36%，明显高于其他胃肠道疾病患者[2] 。细菌脂多糖（LPS）是革兰阴性菌的内毒素，在感染/炎症的发病机制中起着十分重要的作用。Toll蛋白家族在结构上有高度同源性,且均在天然免疫防御中起重要作用。目前有报道的TLR已达10种，其中TLR4多分布在巨噬细胞，B/T淋巴细胞及脾，肝，肺及胎盘等组织中，主要识别革兰氏阴性细菌表面的脂多糖（LPS），引起核转录因子NF-κB的活化及炎症因子的释放[3]。因此,笔者设计动物实验来研究实验性溃疡性结肠炎小鼠的血