Opioid receptors located in the central nervous system and periphery are activated by opioids, which are classified as analgesics and non-analgesics. While investigations show opioids may have more severe consequences on inflammation and neuroinflammation due to down-regulation of cellular functions, these findings remain debatable. With these controversial implications at the forefront, we chose to investigate the fentanyl- and morphine-mediated effects on LPS-induced TLR4 neuroinflammatory signaling. CHME-5 microglial cells treated with LPS induced mu opioid receptor gene expression. Co-treatment with LPS and fentanyl or morphine significantly decreased LPS-induced IÎºBÎ± activation, while only fentanyl decreased NF-ÎºB binding activity. Furthermore, treatment with naltrexone did not reverse the fentanyl-mediated down-regulation of NF-ÎºB binding activity. These findings indicate that fentanyl, and to a lesser extent morphine, display anti-inflammatory effects on LPS-induced TLR4 signaling.
|Original language||American English|
|Journal||Oklahoma State Medical Proceedings|
|State||Published - 8 Nov 2019|