摘要
AIM To investigate the influence of lipopolysaccharide（LPS） through the p38/c-Jun N-terminal kinase （JNK）signalling pathway on aquaporin 3 （AQP3） expressionin HT-29 human colon epithelial cells.METHODS： HT-29 cells were treated with LPS, andthen the membrane localisation of AQP3 was examinedby immunofluorescence staining. The mRNA andprotein expression of AQP3 with LPS exposure wasmeasured by real-time reverse transcription-PCR andWestern blot, respectively. Activation of p38 and JNKwas evaluated by detection of phosphorylation ofp38 and JNK using Western blot assay. AQP3 proteinexpression was determined by Western blot in cellsafter treatment with SB203580, a selective p38 MAPKinhibitor, or SP600125, a selective JNK inhibitor.RESULTS： In HT-29 cells, the transcription and proteinexpression of AQP3 were decreased by LPS in adose- and time-dependent manner, the expression ofAQP3 was significantly decreased with the increasedconcentration of LPS, and at a dose of 100 μg/mLLPS, AQP3 mRNA and protein levels were decreasedby a maximum （P 〈 0.05） of 1.51-fold and 1.49-fold,respectively. When cells were treated with 100 μg/mLLPS for 0, 3, 6, 12, and 24 h, the AQP3 mRNA levelwas significantly decreased at an early time point of3 h, and reached about 10% of the control level at24 h post-treatment （P 〈 0.05）. Down-regulation ofAQP3 expression was significantly inhibited by the p38inhibitor （SB203580） and JNK inhibitor （SP600125）.CONCLUSION： p38 and JNK may be promising targetsfor the preservation of AQP3 expression and may bebeneficial to the clinical management of diarrhoea.
