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Updated: Oct 11, 2025
Injections of Lipopolysaccharide into Mice to Mimic Entrance of Microbial-derived Products After Intestinal Barrier Breach
Published on: May 2, 2018
Remimazolam Protects Against LPS-Induced Endotoxicity Improving Survival of Endotoxemia Mice
Xiaolei Liu1, Shaoping Lin1, Yiyue Zhong1
1The Department of Anesthesiology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Abstract:
Remimazolam is a new benzodiazepine of sedative drugs with an ultra-short-acting anesthetic effect, commonly used for critically ill patients (especially septic patients) in intensive care units (ICUs). Although some anesthetics have been reported to show certain anti-inflammatory effects, the role of remimazolam in inflammation is still remained unknown. Here, we studied the effects of remimazolam on macrophage in response to LPS both in vivo and in vitro. Interestingly, compared with LPS treatment group, remimazolam remarkably improved survival rate of endotoxemia mice and decreased the release of LPS-induced inflammatory mediators (such as TNF-α, IL-6, and IL-1β). We further found that remimazolam not only inhibited the activation of MAPK signal pathway at 15 min after LPS treatment but also disturbed Rab5a related TLR4 expression at cell surface in response to LPS at a later time. Such evidence suggests that remimazolam might be beneficial to septic patients who are suffering from uncontrolled inflammatory responses.
Insights
Remimazolam, a sedative anesthetic, improved survival in endotoxemia mice by reducing inflammatory mediators. It also inhibited MAPK signaling and TLR4 expression, suggesting benefits for septic patients.
Area of Science:
- Pharmacology
- Immunology
- Critical Care Medicine
Background:
- Remimazolam is an ultra-short-acting benzodiazepine anesthetic used in intensive care units.
- The anti-inflammatory role of remimazolam, particularly in sepsis, remains largely unknown.
- Sepsis involves uncontrolled inflammatory responses, necessitating novel therapeutic strategies.
Purpose of the Study:
- To investigate the effects of remimazolam on macrophage responses to lipopolysaccharide (LPS) in vivo and in vitro.
- To determine remimazolam's impact on inflammatory mediator release and survival in an endotoxemia model.
- To elucidate the molecular mechanisms underlying remimazolam's potential anti-inflammatory actions.
Main Methods:
- In vivo studies using endotoxemia mouse models treated with LPS and remimazolam.
- In vitro studies assessing remimazolam's effects on macrophages stimulated with LPS.
- Measurement of inflammatory mediators (TNF-α, IL-6, IL-1β), analysis of MAPK pathway activation, and assessment of TLR4 expression.
Main Results:
- Remimazolam significantly improved survival rates in endotoxemia mice compared to LPS treatment alone.
- Remimazolam markedly decreased the release of key inflammatory mediators, including TNF-α, IL-6, and IL-1β.
- Remimazolam inhibited MAPK pathway activation early after LPS challenge and affected Rab5a-related TLR4 expression later.
Conclusions:
- Remimazolam demonstrates significant anti-inflammatory and survival-promoting effects in an endotoxemia model.
- The drug modulates both early (MAPK) and later (TLR4) inflammatory signaling pathways.
- Remimazolam holds potential as a beneficial therapeutic agent for septic patients experiencing hyperinflammation.
