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Updated: Jun 20, 2026
Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis
Published on: December 9, 2022
Protective effects of remifentanil on septic mice
Zhang Zongze1, Zhan Jia, Chen Chang
1Department of Anesthesiology, Zhongnan Hospital of Wuhan University, East-lake Road 169, 430071 Wuhan, Hubei, China.
Abstract:
This study is to explore the effect of remifentanil on inducible nitric oxide synthase (iNOS) expression, IL-6 and IL-10 levels, myeloperoxidase (MPO) activity, white blood cell count in bronchoalveolar (BALF), ALT and AST activity in septic mice. Forty male KM mice were randomly divided into four groups, sham group, cecal ligation and puncture group (CLP group), remifentanil treatment group (R1 group), and remifentanil control group (R2 group). The mouse model of CLP was used to observe ALT and AST activity, white blood cell count in BALF and myeloperoxidase (MPO). IL-6 and IL-10 in lung and liver tissue were assayed by enzyme-linked immunosorbent assay (ELISA). Lung and liver tissues were harvested for determination of iNOS expression by Western blot analysis. The pathologic changes were observed under electron microscope. Compared with sham group, iNOS protein expression, white blood cell count in BALF, ALT and AST activity, MPO activity, IL-6 and IL-10 levels were markedly increased in CLP group. Compared with CLP group, iNOS protein expression, IL-6 and IL-10 levels, white blood cell count in BALF, ALT and AST activity, MPO activity of R1 group were significantly lower. The pathologic changes induced by sepsis were significantly attenuated by remifentanil under electron microscope. Remifentanil could suppress inflammatory responses and inhibit iNOS expression in septic mice. Remifentanil might have a protective effect against sepsis. Its action mechanisms are probably involved in the inhibition of inflammatory factor production and suppression of iNOS expression.
Insights
Remifentanil significantly reduced inflammatory markers, including inducible nitric oxide synthase (iNOS) expression and cytokine levels, in septic mice. This suggests remifentanil may offer protective effects against sepsis by suppressing inflammation.
Area of Science:
- Pharmacology
- Immunology
- Sepsis Research
Background:
- Sepsis is a life-threatening condition characterized by a dysregulated host response to infection.
- Inflammatory mediators, such as inducible nitric oxide synthase (iNOS), IL-6, and IL-10, play critical roles in sepsis pathogenesis.
- Myeloperoxidase (MPO) activity and white blood cell counts are indicators of inflammation and tissue damage.
Purpose of the Study:
- To investigate the effects of remifentanil on key inflammatory markers in a mouse model of sepsis.
- To evaluate the potential protective role of remifentanil against sepsis-induced organ damage.
Main Methods:
- A cecal ligation and puncture (CLP) model was used to induce sepsis in male KM mice.
- Mice were divided into sham, CLP, and remifentanil-treated groups.
- Measurements included iNOS expression, IL-6 and IL-10 levels, MPO activity, white blood cell counts in bronchoalveolar lavage fluid (BALF), and ALT/AST activity in liver and lung tissues.
Main Results:
- CLP significantly increased iNOS expression, IL-6, IL-10, MPO activity, BALF white blood cells, and ALT/AST levels compared to the sham group.
- Remifentanil treatment (R1 group) significantly reduced all measured inflammatory markers and liver enzyme activities compared to the CLP group.
- Electron microscopy revealed attenuated pathological changes in remifentanil-treated mice.
Conclusions:
- Remifentanil effectively suppresses inflammatory responses and inhibits iNOS expression in septic mice.
- Remifentanil demonstrates a potential protective effect against sepsis, likely through the inhibition of inflammatory factor production and iNOS signaling.
