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The Effects of Remifentanil on Expression of High Mobility Group Box 1 in Septic Rats
Kwon Hui Seo1, Jin Woo Choi1, Hong Soo Jung1
1Department of Anesthesiology and Pain Medicine, Saint Vincent's Hospital, The College of Medicine, The Catholic University of Korea, Suwon, Korea.
Abstract:
High mobility group box 1 (HMGB1) is a pivotal mediator of sepsis progression. Remifentanil, an opioid agonist, has demonstrated anti-inflammatory effects in septic mice. However, it is not yet known whether remifentanil affects the expression of HMGB1. We investigated the effects of remifentanil on HMGB1 expression and the underlying mechanism in septic rats. Forty-eight male Sprague-Dawley rats were randomly divided into 3 groups; a sham group, a cecal ligation and puncture (CLP) group, and a CLP with remifentanil treatment (Remi) group. The rat model of CLP was used to examine plasma concentrations of proinflammatory cytokines, tissue HMGB1 mRNA and the activity of nuclear factor (NF)-κB in the liver, lungs, kidneys, and ileum. Pathologic changes and immunohistochemical staining of NF-κB in the liver, lungs, and kidneys tissue were observed. We found that remifentanil treatment suppressed the level of serum interleukin (IL)-6 and tumor necrosis factor (TNF)-α 6 hours after CLP, and serum HMGB1 24 hours after CLP. HMGB1 mRNA levels and the activity of NF-κB in multiple organs decreased by remifentanil treatment 24 hours after CLP. Remifentanil treatment also attenuated nuclear expression of NF-κB in immunohistochemical staining and mitigated pathologic changes in multiple organs. Altogether, these results suggested that remifentanil inhibited expression of HMGB1 in vital organs and release of HMGB1 into plasma. The mechanism was related to the inhibitory effect of remifentanil on the release of proinflammatory cytokines and activation of NF-κB.
Insights
Remifentanil, an opioid, reduces High mobility group box 1 (HMGB1) in sepsis by inhibiting inflammation and NF-κB activation. This study reveals remifentanil
Area of Science:
- Sepsis Pathophysiology
- Pharmacology
- Immunology
Background:
- High mobility group box 1 (HMGB1) is a key mediator in sepsis progression.
- Remifentanil, an opioid agonist, exhibits anti-inflammatory properties in preclinical models.
- The effect of remifentanil on HMGB1 expression in sepsis remains unelucidated.
Purpose of the Study:
- To investigate the impact of remifentanil on HMGB1 expression in a rat model of sepsis.
- To elucidate the underlying mechanisms by which remifentanil influences HMGB1 and inflammation.
Main Methods:
- A cecal ligation and puncture (CLP) rat model was employed.
- Groups included sham, CLP, and CLP with remifentanil treatment.
- Measurements included serum cytokines, tissue HMGB1 mRNA, NF-κB activity, and histopathology.
Main Results:
- Remifentanil suppressed serum IL-6 and TNF-α levels post-CLP.
- Remifentanil treatment reduced serum HMGB1, tissue HMGB1 mRNA, and NF-κB activation in multiple organs.
- Histopathological analysis showed mitigated organ damage with remifentanil.
Conclusions:
- Remifentanil inhibits the expression and plasma release of HMGB1 in septic rats.
- The mechanism involves suppressing proinflammatory cytokine release and NF-κB activation.
- Remifentanil demonstrates potential therapeutic benefits in sepsis by modulating HMGB1.
