DPP4 inhibitor reinforces cell junction proteins in mouse model of short bowel syndrome.
DPP4 inhibitor reinforces cell junction proteins in mouse model of short bowel syndrome.
复制标题
DPP4 抑制剂增强短肠综合征小鼠模型中的细胞连接蛋白。
DOI：
10.1007/s00383-019-04571-5
复制
发表时间：
2020
影响因子：
1.8
通讯作者：
Yamataka A.
中科院分区：
文献类型：
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作者：
Sueyoshi R;Miyahara K;Nakazawa-Tanaka N;Fujiwara N;Ochi T;Yamataka A.
目的短肠综合征（SBS）常发生细菌过度生长，并易发生细菌移位。胰高血糖素样肽-2（GLP-2）可有效治疗SBS，但会被二肽基肽酶IV（DPP 4）迅速灭活。已知DPP 4抑制剂（DPP 4 I）可有效治疗SBS。在这里，我们研究了细胞连接蛋白功能DPP 4 I管理在小鼠模型SBS.MethodsMice被分为四组：天真（n= 5），天真+DPP 4 I（n= 6），控制（n= 6），和DPP 4 I（n= 5）。所有对照和DPP 4 I小鼠的近端小肠切除50%。术后第1-7天口服DPP 4 I或生理盐水，每日2次。RT-PCR和免疫组化检测细胞连接蛋白的功能。体重和血糖水平recorded.ResultsE-Cadherin是显着高于DPP 4 I组比对照组。E-钙粘蛋白，occludin，和claudin-4显着高于在未处理组比对照组。E-cadherin和occludin的阳性染色在对照组和DPP 4 I组之间差异很大。结论DPP 4 I上调E-cadherin和occludin的表达可能与DPP 4 I的抗炎作用有关。因此，DPP 4 I可减少SBS中的细菌移位。
PurposeBacterial overgrowth commonly occurs and favors bacterial translocation in short bowel syndrome (SBS). Glucagon-like peptide-2 (GLP-2) is effective for treating SBS, but is rapidly inactivated by dipeptidyl peptidase IV (DPP4). DPP4 inhibitor (DPP4I) is known to be effective for treating SBS. Here, we investigated cell junction protein function following DPP4I administration in a mouse model of SBS.MethodsMice were divided into four groups: naïve (n= 5), naïve + DPP4I (n= 6), control (n= 6), and DPP4I (n= 5). All control and DPP4I mice had 50% of their proximal small bowel resected. DPP4I or normal saline was administered orally twice daily from days 1–7 postoperatively. The functions of cell junction proteins were assessed by RT-PCR and immunohistochemistry. Body weights and blood glucose levels were recorded.ResultsE-Cadherin was significantly higher in the DPP4I group than in the control group. E-Cadherin, occludin, and claudin-4 were significantly higher in the naïve group than in the control group. Positive staining for E-cadherin and occludin varied widely between the control and DPP4I groups.ConclusionUp-regulation of E-cadherin and occludin by DPP4I may be correlated with the anti-inflammatory action of DPP4I. Therefore, DPP4I may reduce bacterial translocation in SBS.