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目的探讨实验性末端回肠炎TLR2、TLR4变化及双歧杆菌干预下的表达,研究双歧杆菌对末端回肠黏膜的保护作用及其机制。方法清洁级SD雄性大鼠120只,随机分为6组:正常对照组(A)、模型对照组造模组(B)、缝线组(H)及双岐杆菌低剂量干预组(C)、中剂量干预组(D)、高剂量干预组(E);观察各组大鼠末端回肠黏膜的形态学变化,包括肉眼及病理学评分(histopathological score,HS),免疫组化法检测TLR2,TLR4的表达,进行统计学分析。结果 (1)肉眼及病理学观察,模型对照组与各组相比,炎症评分有显著性差异(P<0.05)。(2)造模组肠上皮细胞TLR2和TL R4的平均吸光度值较其余5组高(P<0.05)。(3)实验性末端回肠炎炎症程度与TLR2和TLR4相关性,末端回肠组织炎症越重,TLR2、TLR4的表达率越高。(4)双歧杆菌的保护作用,干预组TLR2和TLR4的平均吸光度值低于模型组(P<0.05)。结论双歧杆菌可降低末端回肠的炎症反应,对实验性末端回肠炎的保护作用,可能是通过降低TLR2、TLR4的表达得以实现的。
Objective To investigate the changes of TLR2 and TLR4 in experimental terminal ileitis and the expression of TLR2 in Bifidobacterium and to study the protective effect of Bifidobacterium on the terminal ileum mucosa and its mechanism. Methods 120 male Sprague Dawley rats were randomly divided into 6 groups: normal control group (A), model control group (B), suture group (H) and Bifidobacterium low dose intervention group (C) , Medium dose intervention group (D), and high dose intervention group (E). Morphological changes of terminal ileum mucosa were observed in all groups, including histopathological score (HS), immunohistochemistry staining for TLR2, TLR4 expression, statistical analysis. Results (1) Macroscopic and pathological observation, the model control group compared with each group, the inflammation score was significantly different (P <0.05). (2) The average absorbance values of TLR2 and TL R4 in intestinal epithelial cells of model group were higher than those of the other 5 groups (P <0.05). (3) The correlation between inflammatory degree of experimental terminal ileitis and TLR2 and TLR4, the more serious inflammation of terminal ileum, the higher the expression rate of TLR2 and TLR4. (4) The protective effect of Bifidobacterium, the average absorbance of TLR2 and TLR4 in intervention group was lower than that in model group (P <0.05). Conclusions Bifidobacterium can reduce the inflammatory reaction in the terminal ileum. The protective effect on experimental terminal ileitis may be achieved by reducing the expression of TLR2 and TLR4.