Evidence map›Paper›PMID 36724020›Full record

ArticleBiomolecules & biomedicine2023

Sivelestat sodium attenuates acute lung injury by inhibiting JNK/NF-κB and activating Nrf2/HO-1 signaling pathways.

Hong Zhang, Jun Zeng, Jiankang Li, Huankai Gong, Meiling Chen, Quan Li, Shengxing Liu, Shanjun Luo, Huanxiang Dong, Yingke Xu and 3 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomolecules & biomedicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 18 citations in OpenAlex.

  1. Pooled it
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  11. Total flavonoids ofIranian journal of basic medical sciences · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 1 country.

Hong ZhangEmergency and Trauma College, Hainan Medical University, Haikou, Hainan, China; Key Laboratory of Emergency and Trauma of Ministry of Education, Hainan Medical University, Haikou, Hainan, China.
Jun ZengEmergency Medicine Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Jiankang LiEmergency and Trauma College, Hainan Medical University, Haikou, Hainan, China; Key Laboratory of Emergency and Trauma of Ministry of Education, Hainan Medical University, Haikou, Hainan, China.
Huankai GongEmergency and Trauma College, Hainan Medical University, Haikou, Hainan, China; Key Laboratory of Emergency and Trauma of Ministry of Education, Hainan Medical University, Haikou, Hainan, China.
Meiling ChenEmergency and Trauma College, Hainan Medical University, Haikou, Hainan, China; Key Laboratory of Emergency and Trauma of Ministry of Education, Hainan Medical University, Haikou, Hainan, China.
Quan LiDepartment of Emergency, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.
Shengxing LiuDepartment of Orthopedics, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan, China.
Shanjun LuoIntensive Care Unit, Chenzhou Third People's Hospital, Chenzhou, Hunan, China.
Huanxiang DongEmergency and Trauma College, Hainan Medical University, Haikou, Hainan, China; Key Laboratory of Emergency and Trauma of Ministry of Education, Hainan Medical University, Haikou, Hainan, China.
Yingke XuEmergency and Trauma College, Hainan Medical University, Haikou, Hainan, China; Key Laboratory of Emergency and Trauma of Ministry of Education, Hainan Medical University, Haikou, Hainan, China.
Huanling DuanEmergency and Trauma College, Hainan Medical University, Haikou, Hainan, China; Key Laboratory of Emergency and Trauma of Ministry of Education, Hainan Medical University, Haikou, Hainan, China.
Ling HaungHainan Pharmacopoeia Review Center of Hainan Provincial Drug Administration, Haikou, Hainan, China; State Key Laboratory of Trauma, Burns and Combined Injury, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, China; Research Center for Drug Safety Evaluation of Hainan Province, Hainan Medical University, Haikou, Hainan, China.
Chuanzhu LvKey Laboratory of Emergency and Trauma of Ministry of Education, Hainan Medical University, Haikou, Hainan, China; Emergency Medicine Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China; Research Unit of Island Emergency Medicine, Chinese Academy of Medical Sciences (No. 2019RU013), Hainan Medical University, Haikou, Hainan, China.
Hainan Medical University · CNUniversity of Electronic Science and Technology of China · CNArmy Medical University · CNChenzhou First People's Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sivelestat sodium (SIV), a neutrophil elastase inhibitor, is mainly used for the clinical treatment of acute respiratory distress syndrome (ARDS) or acute lung injury (ALI). However, studies investigating the effects of SIV treatment of ALI are limited. Therefore, this study investigated the potential molecular mechanism of the protective effects of SIV against ALI. Human pulmonary microvascular endothelial cells (HPMECs) were stimulated with tumor necrosis factor α (TNF-α), and male Sprague-Dawley rats were intratracheally injected with Klebsiella pneumoniae (KP) and treated with SIV, ML385, and anisomycin (ANI) to mimic the pathogenetic process of ALI in vitro and in vivo, respectively. The levels of inflammatory cytokines and indicators of oxidative stress were assessed in vitro and in vivo. The wet/dry (W/D) ratio of lung tissues, histopathological changes, inflammatory cells levels in bronchoalveolar lavage fluid (BALF), and survival rates of rats were analyzed. The JNK/NF-κB (p65) and Nrf2/HO-1 levels in the HPMECs and lung tissues were analyzed by western blot and immunofluorescence analyses. Administration of SIV reduced the inflammatory factors levels, intracellular reactive oxygen species (ROS) production, and malondialdehyde (MDA) levels and increased the levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in lung tissues. Meanwhile, SIV alleviated pathological injuries, decreased the W/D ratio, and inflammatory cell infiltration in lung tissue. In addition, SIV also inhibited the activation of JNK/NF-κB signaling pathway, promoted nuclear translocation of Nrf2, and upregulated the expression of heme oxygenase 1 (HO-1). However, ANI or ML385 significantly reversed these changes. SIV effectively attenuated the inflammatory response and oxidative stress. Its potential molecular mechanism was related to the JNK/NF-κB activation and Nrf2/HO-1 signaling pathway inhibition. This further deepened the understanding of the protective effects of SIV against ALI.

Indexed as

Acute Lung InjuryNF-kappa BAnimalsEndothelial CellsGlycineHeme Oxygenase-1HumansMaleMAP Kinase Kinase 4NF-E2-Related Factor 2RatsRats, Sprague-DawleySignal TransductionSodiumSulfonamidesGlycineHeme Oxygenase-1MAP Kinase Kinase 4NF-E2-Related Factor 2NF-kappa BsivelestatSodiumSulfonamides

Identifiers

PMID36724020
PMCPMC10171443
OpenAlexW4313521099

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.