New Modes of GPCR Signalling
New Modes of GPCR Signalling
New Modes of GPCR Signalling
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Morphine Regulated Thioredoxin-1 Expression<br />
in Neuroblastoma SH-SY5Y Cells<br />
Yuemei Feng, Kui Li, Shengdong Wang, Yanhui Li, Junying Song, Fucheng Luo, Jie<br />
Bai*<br />
College <strong>of</strong> life science and technology, Kunming University <strong>of</strong> Science and Technology,<br />
Kunming 650224, China<br />
Aim: Thioredoxin-1 (TRX-1) plays multiple roles in regulation <strong>of</strong> redox, inhibition <strong>of</strong><br />
apoptosis and regulation <strong>of</strong> transcription factors. Recent studies showed that morphine<br />
could cause oxidative stress in cells and tissues. The aim <strong>of</strong> current study is to<br />
investigate the expression <strong>of</strong> TRX-1 under morphine administration in human<br />
neuroblastoma SH-SY5Y cells. Methods: Cell culture, Western blotting. Results: The<br />
expression <strong>of</strong> TRX-1 was decreased after 1-2h then increased from 4 -24h after<br />
morphine treatment in human neuroblastoma SH-SY5Y. The decreased expression <strong>of</strong><br />
TRX-1 by morphine was restored by an inhibitor <strong>of</strong> GSK3β, lithium chloride. The<br />
increased expression <strong>of</strong> TRX-1 induced by morphine was suppressed by LY294002,<br />
which is one <strong>of</strong> the PI3K inhibitor and was suppressed by the antagonist <strong>of</strong> opioid<br />
receptor, naloxone. The increased expression <strong>of</strong> TRX-1 recovered to normal level after<br />
morphine withdrawal. These data suggested that TRX-1 was induced through the opioid<br />
receptor and the PI3K/GSK3β pathway. The expression <strong>of</strong> TRX-1 is dependent on the<br />
morphine administration. Conclusion: Our study suggested that TRX-1 might be<br />
associated with morphine tolerance and abuse.<br />
Key words: thioredoxin-1, morphine, neuroblastoma SH-SY5Y cells<br />
*Author for correspondence: Tel.: +86 13354980126; fax: +86 8713801191, E-mail:<br />
jiebai662001@yahoo.com.cn