Evidence map›Paper›PMID 25550770›Full record

ArticleInternational journal of clinical and experimental pathology2014

Ulinastatin inhibits oxidant-induced endothelial hyperpermeability and apoptotic signaling.

Guicheng Li, Tao Li, Yunfeng Li, Shumin Cai, Zhiming Zhang, Zhenhua Zeng, Xingmin Wang, Youguang Gao, Yunfeng Li, Zhongqing Chen

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 24% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Observational
  4. Article
  5. Review
  6. Efficacy of Ulinastatin and Sulforaphane Alone or in Combination in Rat Model of Streptozotocin Diabetes Induced Vascular Dementia.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2021
    Article
  7. Review
  8. Article
  9. Observational
  10. [Effect of ulinastatin on isoflurane-induced neuronal apoptosis in the hippocampus of rats].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Nickel-Refining Fumes Induced DNA Damage and Apoptosis of NIH/3T3 Cells via Oxidative Stress.International journal of environmental research and public health · 2016
    Article
  16. Article
  17. Ulinastatin mediates protection against vascular hyperpermeability following hemorrhagic shock.International journal of clinical and experimental pathology · 2015
    Article
  18. 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

10 authors at 4 institutions in 1 country.

Guicheng LiDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University Guangzhou, China ; Department of Critical Care Medicine, The First People's Hospital of Chenzhou, Institute of Translation Medicine Chenzhou, China.
Tao LiDepartment of Critical Care Medicine, The First People's Hospital of Chenzhou, Institute of Translation Medicine Chenzhou, China.
Yunfeng LiDepartment of Critical Care Medicine, The First People's Hospital of Chenzhou, Institute of Translation Medicine Chenzhou, China.
Shumin CaiDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University Guangzhou, China.
Zhiming ZhangDepartment of Anesthesiology, The First People's Hospital of Chenzhou, Institute of Translation Medicine Chenzhou, China.
Zhenhua ZengDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University Guangzhou, China ; Guangdong Key Lab of Shock and Microcirculation Research, Department of Pathophysiology, Southern Medical University Guangzhou, China.
Xingmin WangDepartment of Pathology, Maternal and Child Health Hospital of Liuzhou Liu Zhou, China.
Youguang GaoDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University Guangzhou, China ; Department of Anesthesiology, The First Affiliated Hospital of Fujian Medical University Fuzhou, China.
Yunfeng LiDepartment of Critical Care Medicine, The First People's Hospital of Chenzhou, Institute of Translation Medicine Chenzhou, China.
Zhongqing ChenDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University Guangzhou, China.
Chenzhou First People's Hospital · CNSouthern Medical University · CNFujian Medical University · CNLiuzhou Maternal and Child Health Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidants are important signaling molecules known to increase endothelial permeability. Studies implicate reactive oxygen species (ROS) and the intrinsic apoptotic signaling cascades as mediators of vascular hyperpermeability. Here we report the protective effects of ulinastatin, a serine protease inhibitor with antiapoptotic properties, against oxidant-induced endothelial monolayer hyperpermeability. HUVECs were respectively pretreated with 10,000 and 50,000 u/l ulinastatin, followed by stimulation of 0.6 mM H₂O₂. Monolayer permeability was determined by transendothelial electrical resistance (TER); Mitochondrial release of cytochrome c was determined by enzyme-linked immunosorbent assay; Caspase-3 activity was measured by fluorometric assay; Adherens junction protein β-catenin was detected by immunofluorescense staining; Ratio of cell apoptosis was evaluated by Annexin-V/PI double stain assay; Mitochondrial membrane potential (Δψm) was determined with JC-1; Intracellular ATP content was assayed by a commercial kit; Bax and Bcl-2 expression were estimated by western blotting; Intracellular reactive oxygen species (ROS) level was measured by DCFH-DA. H₂O₂ exposure resulted in endothelial hyperpermeability and ROS formation (P < 0.05). The activation of mitochondrial intrinsic apoptotic signaling pathway was evidenced from BAX up-regulation, Bcl-2 down-regulation, mitochondrial depolarization, an increase in cytochrome c release, and activation of caspase-3 (P < 0.05). UTI (50,000 u/l) attenuated endothelial hyperpermeability, ROS formation, mitochondrial dysfunction, cytochrome c release, activation of caspase-3, and disruption of cell adherens junctions (P < 0.05). Together, these results demonstrate that UTI provides protection against vascular hyperpermeability by modulating the intrinsic apoptotic signaling.

Indexed as

Adherens JunctionsApoptosisBenzimidazolesbeta CateninCarbocyaninesCaspase 3Cell Membrane PermeabilityCytochromes cDown-RegulationEndothelial CellsEnzyme-Linked Immunosorbent AssayGlycoproteinsHumansMembrane Potential, MitochondrialMitochondriaReactive Oxygen Species5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolocarbocyanineBenzimidazolesbeta CateninCarbocyaninesCaspase 3Cytochromes cGlycoproteinsReactive Oxygen SpeciesSerine Proteinase Inhibitorsurinastatinadherens junctionsapoptosisEndothelial barriermitochondriaoxidative stress

Identifiers

PMID25550770
PMCPMC4270631
OpenAlexW2412399358

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.