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

**Authors:** Xiaoxin Gao, Rujun Zhang, Zhenzhou Wang, Qingan Chen, Zhenlin Lei, Yanan Yang, Jia Tian

PMC · DOI: 10.7717/peerj.17205 · PeerJ · 2024-04-18

## TL;DR

This study shows that remazolam may help protect against lung damage caused by sepsis by reducing inflammation and improving immune function.

## Contribution

The study demonstrates remazolam's protective effects against sepsis-induced ARDS by reducing HMGB1 expression and inflammation.

## Key findings

- Remazolam improved alveolar structure and reduced lung edema in sepsis-induced ARDS.
- Remazolam decreased proinflammatory markers and increased immune cell levels in septic rats.
- HMGB1 protein expression was significantly reduced in the remazolam-treated sepsis group.

## Abstract

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.

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.

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.

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.

## Linked entities

- **Proteins:** HMGB1 (high mobility group box 1)
- **Chemicals:** IL-6 (PubChem CID 165368475), MDA (PubChem CID 1614), MPO (PubChem CID 3270828), ATP (PubChem CID 5957)
- **Diseases:** acute respiratory distress syndrome (MONDO:0006502), ARDS (MONDO:0006502)

## Full-text entities

- **Genes:** Tnf (tumor necrosis factor) [NCBI Gene 24835] {aka RATTNF, TNF-alpha, Tnfa}, Hmgb1 (high mobility group box 1) [NCBI Gene 25459] {aka Ac2-008, Hmg1}, Crp (C-reactive protein) [NCBI Gene 25419] {aka Aa1249, Ab1-341, Ab2-196, Ac1-114, Ac1262, Ac2-069}, Cd4 (Cd4 molecule) [NCBI Gene 24932] {aka W3/25, p55}, Il6 (interleukin 6) [NCBI Gene 24498] {aka ILg6, Ifnb2}, Il1b (interleukin 1 beta) [NCBI Gene 24494] {aka IL-1F2}, Mpo (myeloperoxidase) [NCBI Gene 303413]
- **Diseases:** infected (MESH:D007239), lung damage (MESH:D008171), inflammatory (MESH:D007249), ARDS (MESH:D012128), lung edema (MESH:D004487), lung injury (MESH:D055370), Sepsis (MESH:D018805)
- **Chemicals:** ATP (MESH:D000255), HE (MESH:D006371), PCO2 (-), MDA (MESH:D015104)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC11032653/full.md

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11032653/full.md

## References

28 references — full list in the complete paper: https://tomesphere.com/paper/PMC11032653/full.md

---
Source: https://tomesphere.com/paper/PMC11032653