Evidence map›Paper›PMID 31932743›Full record

ArticleScientific reports2020

Rolipram Protects Mice from Gram-negative Bacterium Escherichia coli-induced Inflammation and Septic Shock.

Xiaying Lu, Juan Wang, Xiaohuan Chen, Yong Jiang, Zhixing K Pan

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04570449 (Fluoxetine to Reduce Hospitalization From COVID-19 Infection), which is not on this map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 28% 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.

NCT04570449 early_phase1withdrawnnot on this map

Fluoxetine to Reduce Hospitalization From COVID-19 Infection (FloR COVID-19)

TypeinterventionalSponsorMilton S. Hershey Medical CenterRan2020 to 2021Enrolled0ConditionsCovid19ArmsFluoxetine, Placebo
3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 16 citations in OpenAlex.

  1. EartEarthworm hydrolysate alleviatesFrontiers in microbiology · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Fluoxetine as an anti-inflammatory therapy in SARS-CoV-2 infection.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Article
  7. Article
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

5 authors at 2 institutions in 2 countries.

Xiaying LuDepartment of Pathophysiology and Key Laboratory of Proteomics of Guangdong Province, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Juan WangDepartment of Pathophysiology and Key Laboratory of Proteomics of Guangdong Province, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Xiaohuan ChenDepartment of Medical Microbiology and Immunology, University of Toledo Medical Center, Toledo, Oh, 43614, USA.
Yong JiangDepartment of Pathophysiology and Key Laboratory of Proteomics of Guangdong Province, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China. jiang48231@163.com.ORCID http://orcid.org/0000-0002-8087-5717
Zhixing K PanDepartment of Medical Microbiology and Immunology, University of Toledo Medical Center, Toledo, Oh, 43614, USA. kevin.pan@utoledo.edu.
Southern Medical University · CNUniversity of Toledo Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is typically triggered by an overwhelming systemic inflammatory response to pathogens, and may lead to severe organ dysfunction and/or death. Sepsis consequently has a high mortality rate and a high rate of complications for survivors, despite modern medical advances. Therefore, drug identification and validation for the treatment of sepsis is of the utmost importance. As a selective phosphodiesterase-4 inhibitor, rolipram also exhibits the abilities of inhibiting multiple pro-inflammatory cytokines production in macrophages and toxin-induced inflammation in mice. However, this drug has never been studied as a sepsis treatment method. We found that rolipram significantly improves survival in mice challenged with gram-negative bacterium E. coli, CLP, or E. coli derived lipopolysaccharide. We have also found that rolipram inhibits organ damage, pro-inflammatory cytokine production, and intracellular migration of early-stage inflammatory elements. Our results also show that rolipram increases anti-inflammatory cytokine production. The protective effects of rolipram on septic mice may result from inhibition of the MAP kinase and NF-κB signaling pathways. Rolipram may therefore be a potential novel sepsis treatment, one that would bypass the time-consuming and costly drug-discovery process.

Indexed as

AnimalsAnti-Inflammatory AgentsCytokinesEscherichia coliEscherichia coli InfectionsInflammationLipopolysaccharidesMacrophagesMaleMiceMice, Inbred C57BLNF-kappa BPhosphodiesterase 4 InhibitorsProtective AgentsRolipramShock, SepticAnti-Inflammatory AgentsCytokinesLipopolysaccharidesNF-kappa BPhosphodiesterase 4 InhibitorsProtective AgentsRolipram

Identifiers

PMID31932743
PMCPMC6957694
OpenAlexW2998829557

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.