肠三叶因子对内毒素血症幼鼠肠组织Toll样受体2和4表达的影响

Effects of intestinal trefoil factor on Toll-like receptors 2 and 4 expression in intestinal tissue in young rats with endotoxemia

摘要:

目的：探讨肠三叶因子对内毒素血症幼鼠肠组织Toll样受体（TLR）2、4表达的调节及对肠组织损伤的影响。方法：24只10日龄Wistar幼鼠随机分为正常对照组（NS组，n=8，生理盐水1 mL/kg腹腔注射）；内毒素血症组（LPS组，n=8，LPS 5 mg/kg 腹腔注射）；肠三叶因子组（ITF组，n=8，重组肠三叶因子 0.1 mL/只＋LPS 5 mg/kg腹腔注射）。于腹腔注射后3 h处死，留取远端回肠组织观察肠组织病理改变，RT-PCR检测肠组织TLR2、4-mRNA的表达。结果：光镜下NS组肠组织结构正常，ITF组和LPS组均可见间质和上皮细胞水肿，ITF组较LPS组病变明显减轻。ITF组肠组织TLR2 mRNA 表达较NS组、LPS组明显增高（P＜0.01）； 而TLR4 mRNA表达较NS组和LPS组明显下降（P＜0.01）。结论：肠三叶因子可减轻内毒素血症幼鼠肠组织损伤，这种保护作用可能与其下调TLR4 mRNA的表达相关。

Abstract:

OBJECTIVE: To study the effects of intestinal trefoil factor (ITF) on Toll-like receptors (TLR) 2 and 4 expression in intestinal tissue and on intestinal injury in young rats with endotoxemia. METHODS: A total of 24 10-day-old Wistar rat pups were equally randomly divided into three groups: a control group, intraperitoneally injected with normal saline 1 mL/kg; an endotoxemia group, intraperitoneally injected with lipopolysaccharide (LPS) 5 mg/kg and an ITF group,intraperitoneally injected with rITF 0.1 mL/each plus LPS 5 mg/kg. Rats were sacrificed 3 h after injection. A segment of distal ileum was dissected for pathologic examinations under an optical microscope (hematoxylin-eosin staning). The mRNA expressions of TLR2 and TLR4 were detected by reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: The structure of the small intestine remained normal in the control group. Edema of interstitial substance and epithelium were observed in both LPS and ITF groups, whereas such changes were significantly lower in the ITF group than in the LPS group. The ITF group had significantly higher TLR2 mRNA expression than the NS and LPS groups (P＜0.01), whereas the mRNA expression of TLR4 in the ITF group was significantly lower than in the NS and LPS groups (both P＜0.01). CONCLUSIONS: ITF can alleviate intestinal injury in young rats with endotoxemia, which may be related to the down-regulation of TLR4 mRNA expression.