丙磺舒直接损害犬P2X7受体的激活。
Probenecid directly impairs activation of the canine P2X7 receptor.
作者信息
Bartlett Rachael, Stokes Leanne, Curtis Stephen J, Curtis Belinda L, Sluyter Ronald
机构信息
a School of Biological Sciences, University of Wollongong , Wollongong , NSW , Australia.
b Centre for Medical and Molecular Bioscience, University of Wollongong , Wollongong , NSW , Australia.
出版信息
Nucleosides Nucleotides Nucleic Acids. 2017 Dec 2;36(12):736-744. doi: 10.1080/15257770.2017.1391395. Epub 2017 Dec 4.
The current study aimed to determine if probenecid could directly impair the canine P2X7 receptor, a ligand-gated cation channel activated by extracellular adenosine 5'-triphosphate (ATP). Patch clamp measurements demonstrated that probenecid impairs ATP-induced inward currents in HEK-293 cells expressing canine P2X7. Flow cytometric measurements of ethidium uptake into HEK-293 cells expressing canine P2X7 showed that probenecid impairs ATP-induced pore formation in a concentration-dependent manner, with a half maximal inhibitory concentration of 158 µM. Finally, ELISA measurements revealed that probenecid impairs ATP-induced interleukin-1β release in dog blood. In conclusion, this study reveals that probenecid can directly impair canine P2X7 activation.
本研究旨在确定丙磺舒是否能直接损害犬P2X7受体，该受体是一种由细胞外三磷酸腺苷（ATP）激活的配体门控阳离子通道。膜片钳测量表明，丙磺舒会损害表达犬P2X7的HEK-293细胞中ATP诱导的内向电流。对表达犬P2X7的HEK-293细胞摄取溴化乙锭的流式细胞术测量显示，丙磺舒以浓度依赖的方式损害ATP诱导的孔形成，半数最大抑制浓度为158 μM。最后，酶联免疫吸附测定显示，丙磺舒会损害犬血液中ATP诱导的白细胞介素-1β释放。总之，本研究表明丙磺舒可直接损害犬P2X7的激活。
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