Aquaporins 1, 3 and 8 expression in irritable bowel syndrome rats' colon via NF-κB pathway.

Aquaporins 1, 3 and 8 expression in irritable bowel syndrome rats' colon via NF-κB pathway.
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肠易激综合症大鼠结肠的含水通道蛋白1、3和8通过NF-κB途径表达。

DOI:
10.18632/oncotarget.17565
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发表时间:
2017-07-18
期刊:
影响因子:
--
通讯作者:
Zhang S
Zhang S
中科院分区:
其他
文献类型:
--
作者:
Chao G;Zhang S

文献摘要

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本研究旨在检测水通道蛋白的表达。目的研究NF-κB在肠易激综合征(IBS)大鼠模型结肠中的表达,以期发现IBS新的发病机制。与对照组相比,IBS模型组AQP 1、AQP 3、AQP 8表达下调,NF-κB p65表达上调(p < 0.05);与IBS模型组相比,抑制剂组AQP 1、AQP 3、AQP 8表达上调,NF-κB p65表达下调(p < 0.05)。将18只成年雌性SD大鼠随机分为正常对照组、IBS模型组和抑制剂组,每组18只,分别给予NF-κB抑制剂(PDTC)注射。采用免疫组化和western blot检测AQP 1、AQP 3、AQP 8和NF-κB p65的表达。RT-PCR检测AQP 1、AQP 3和AQP 8的表达。肠易激综合征的发病机制可能是通过NF-κB途径下调AQP 1、AQP 3和AQP 8的表达而引起的。
Our research was to detect the expression of aquaporins. NF-κB in Irritable bowel syndrome (IBS) rat models’ colon so as to find novel pathogenesisof IBS. The expression of AQP1, AQP3, and AQP8 of IBS model group was down-regulated while NF-κB p65 was up-regulated comparing with control group (p < 0.05), and the expression of AQP1, AQP3, and AQP8 of inhibitor group was up-regulated while NF-κB p65 was down-regulated comparing with IBS model group (p < 0.05). 18 adult female SD big rats were divided into three groups:the rats in control group were normal rats, the rats in IBS model group and the rats of inhibitor group were injected with the inhibitor of NF-κB (PDTC). Immunohistochemical technique and western blot were performed to detect the expression of AQP1, AQP3, AQP8 and NF-κB p65. RT-PCR was performed to detect the expression of AQP1, AQP3, and AQP8. Liquid water metabolic abnormalities and intestine permeability alteration might be the mechanism of IBS by down-regulating AQP1, AQP3 and AQP8 via NF-κB pathway.