Preliminary study on the protective effect of remazolam against sepsis-induced acute respiratory distress syndrome (ARDS)

PeerJ. 2024 Apr 18:12:e17205. doi: 10.7717/peerj.17205. eCollection 2024.

Abstract

Background: Sepsis can disrupt immune regulation and lead to acute respiratory distress syndrome (ARDS) frequently. Remazolam, a fast-acting hypnotic drug with superior qualities compared to other drugs, was investigated for its potential protective effects against sepsis-induced ARDS.

Methods: Forty Sprague-Dawley rats were randomly divided into four groups, including the sepsis + saline group, sham operation + saline group, sham operation + remazolam group and the sepsis + remazolam group. Lung tissues of rats were extracted for HE staining to assess lung damage, and the wet weight to dry weight (W/D) ratio was calculated. The levels of proinflammatory factors, anti-inflammatory factors, CD4+ and CD8+ T cells in peripheral blood, MDA, MPO, and ATP in the lung tissue were measured by using ELISA. Western blotting was performed to determine the protein expression of HMGB1 in lung tissues.

Results: In comparison to the sham operation + saline and sham operation + remazolam groups, the sepsis + saline group exhibited significantly higher values for W/D ratio, lung damage score, IL-1β, IL-6, TNF-α, PCT, CRP, MDP and MPO, while exhibiting lower levels of CD4+ and CD8+ T lymphocytes, PaO2, PCO2, and ATP. The rats in the sepsis + saline group displayed ruptured alveolar walls and evident interstitial lung edema. However, the rats in the sepsis + remazolam group showed improved alveolar structure. Furthermore, the HMGB1 protein expression in the sepsis + remazolam group was lower than the sepsis + saline group.

Conclusion: Remazolam can alleviate the inflammatory response in infected rats, thereby alleviating lung injury and improving immune function, which may be attributed to the reduction in HMGB1 protein expression.

Keywords: ARDS; HMGB1; Immune function; Inflammatory factors; Remazolam; Sepsis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Disease Models, Animal
  • HMGB1 Protein / metabolism
  • Lung / drug effects
  • Lung / immunology
  • Lung / metabolism
  • Lung / pathology
  • Male
  • Rats
  • Rats, Sprague-Dawley*
  • Respiratory Distress Syndrome* / immunology
  • Sepsis* / complications
  • Sepsis* / immunology
  • Sepsis* / metabolism

Substances

  • HMGB1 Protein

Associated data

  • figshare/10.6084/m9.figshare.22638901.v1

Grants and funding

This study was funded by grants from the Medical and Health Research Projects in Hainan Province (2001032099A2011); the Medical and Health Research Projects in Hainan Province (2101032024A2006); the 530 Youth Project of National Natural Science Foundation of Hainan General Hospital (2121QNXM15); and the General Project of Natural Science Foundation of Hainan Province (820MS138). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.