Dexamethasone attenuates LPS-induced changes in expression of urea transporter and aquaporin proteins, ameliorating brain endotoxemia in mice

International Journal of Clinical and Experimental Pathology

Lu Li¹  Shuhua Zhao¹  Xuejiao Lv¹  Zhenzhong Su¹  Lijing Zhao¹  Yanwei Du¹  Xuejian Zhao¹  Yan Meng¹  Lirong Guo¹  Na Li¹  Xiaoqin Wang¹ 

关键词: Lipopolysaccharide (LPS);    urea transporters (UTs);    aquaporins (AQPs);    dexamethasone (Dexa);    brain;   

DOI  :  

学科分类：生理学与病理学

来源: e-Century Publishing Corporation

【 摘 要 】

Aim: AQP4 in the brain is involved in the occurrence and development of a variety of encephalopathy. AQPs family changes in kidney were accompanied by altered UTs family. The aim of this study was to observe AQP4 and UT-A3 expression in CNS and to explore their role in the pathogenesis of endotoxemia encephalopathy following peripheral LPS injection in mice. Methods: Endotoxemia was induced in C57Bl/6 mice by intraperitoneal injection of LPS. The expression of UT-A3 and AQP4 in brain were detected by Western blot and immunohistochemistry, the level of cytokines were detected by ELISA, and the content of LDH, AST/ALT, BUN and CREA were detected by colorimetric method. Results: As compared with the control group, in model group, the brain weight/ body weight ratio increased by 13%. Meanwhile, a 2.5 fold increase in LDH and a 1.2 fold increase in AST/ALT were found in peripheral serum (P < 0.05), and also, BUN and CREA increased 2.5 fold (P < 0.01). In addition to severe CNS injury in response to lipopolysaccharide, the contents of cytokines and the expression of AQP4 protein in hippocampal is increased (P < 0.05), while the expression of UT-A3 protein in the hippocampus and cortical astrocytes decreased (P < 0.05). And, in part, Dexa pretreatment attenuated those effects. Conclusions: In endotoxemia encephalopathy, AQPs and UTs which regulate the functions of cell membrane are both altered. We suggested that the molecular mechanisms of regulation in endotoxemia may provide a new strategy for clinical treatment of the disease and drug binding sites.

【 授权许可】

Unknown