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Published on: August 23, 2022
Posttreatment with propofol attenuates lipopolysaccharide-induced up-regulation of inflammatory molecules in primary
Mian Peng1, Ji-Shi Ye, Yan-Lin Wang
1Department of Anesthesiology, Zhongnan Hospital of Wuhan University, 169, Donghu Road, Wuhan, 430071, China, sophie_pm@msn.com.
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.
Materials And 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.
Insights
Propofol effectively reduces inflammatory responses in activated microglia by inhibiting key inflammatory molecules. This suggests propofol may be beneficial for patients with neuroinflammatory diseases requiring anesthesia.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglial activation is central to neuroinflammation.
- Suppressing microglial activation may slow neuroinflammatory disease progression.
- Propofol exhibits known anti-inflammatory properties.
Purpose of the Study:
- To investigate propofol's effects on inflammatory molecule production in lipopolysaccharide (LPS)-stimulated microglia.
- To assess propofol's potential to mitigate neuroinflammation.
Main Methods:
- Microglia were stimulated with LPS and subsequently treated with varying concentrations of propofol (25–250 μM).
- Levels of nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) were measured.
- Expression of corresponding mRNAs (iNOS, COX-2, TNF-α, IL-1β) was assessed.
Main Results:
- Propofol at 25 μM showed no significant effect on LPS-induced inflammation.
- Concentrations of 50, 100, and 250 μM propofol significantly inhibited LPS-mediated production of NO, PGE2, TNF-α, and IL-1β.
- These concentrations also significantly reduced the mRNA expression of these inflammatory mediators.
Conclusions:
- Propofol effectively reduces inflammatory responses in LPS-induced activated microglia at clinically relevant concentrations.
- Propofol may be a preferred anesthetic for neuroinflammatory patients needing sedation or anesthesia.
- These findings highlight propofol's therapeutic potential in managing neuroinflammatory conditions.
