Posttreatment with propofol attenuates lipopolysaccharide-induced up-regulation of inflammatory molecules in primary microglia.
BACKGROUND
Activation of microglia is involved in a broad range of neuroinflammatory diseases. Suppression of microglial activation may, therefore, contribute to alleviate the progression of neuroinflammatory diseases. It has been reported that propofol has a potent anti-inflammatory property. In the present study, we investigated the effects of posttreatment with propofol on the production of inflammatory molecules in lipopolysaccharide (LPS)-stimulated microglia.


METHODS
Microglia were exposed to various concentrations (25, 50, 100, 250 μM) of propofol for 1 h after LPS stimulation for 24 h. The levels of proinflammatory mediators inducible nitric oxide synthase (iNOS)/nitric oxide (NO), cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were measured.


RESULTS
Propofol at a concentration of 25 μM did not affect the production of proinflammatory mediators, which was enhanced by LPS. At the concentrations of 50, 100, and 250 μM, propofol significantly inhibited LPS-mediated production of NO, PGE2, TNF-α, and IL-1β and the expression of iNOSmRNA, COX-2mRNA, TNF-α mRNA, and IL-1β mRNA.


CONCLUSIONS
These results suggest that propofol, at clinically relevant concentrations, can reduce inflammatory responses in LPS-induced inflammation in activated microglia and might be an intravenous anesthetic of choice when patients with neuroinflammatory diseases require sedation and/or general anesthesia.
Department of Anesthesiology, Zhongnan Hospital of Wuhan University, 169, Donghu Road, Wuhan, 430071, China, sophie_pm@msn.com.
Mian
M
Peng
Ji-Shi
JS
Ye
Yan-Lin
YL
Wang
Chang
C
Chen
Cheng-Yao
CY
Wang
D000818:Animals; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D051546:Cyclooxygenase 2 / Q000235:genetics; D016207:Cytokines / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D018836:Inflammation Mediators / Q000502:physiology*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D017628:Microglia / Q000276:immunology*; D018696:Neuroprotective Agents / Q000494:pharmacology*; D009569:Nitric Oxide / Q000096:biosynthesis; D015742:Propofol / Q000494:pharmacology*; D051381:Rats; D015854:Up-Regulation
D016207:Cytokines; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D018696:Neuroprotective Agents; D009569:Nitric Oxide; D051546:Cyclooxygenase 2; D015742:Propofol