Evidence map›Paper›PMID 30610183›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2019

β-Casomorphin-7 Ameliorates Sepsis-Induced Acute Kidney Injury by Targeting NF-κB Pathway.

ZhiJie Zhang, Huatang Zhao, DongJian Ge, Shanshan Wang, Bin Qi

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. 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
2.7field-weighted citation impact, top 10% 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, 24 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Peptide-Based Approaches for Pain Relief and Healing in Wounds.International journal of molecular sciences · 2026
    Review
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  5. Protective effect ofBiomedical reports · 2025
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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

5 authors at 3 institutions in 1 country.

ZhiJie ZhangDepartment of Anesthesiology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu, China (mainland).
Huatang ZhaoDepartment of Anesthesiology, Taishan Medical University Affiliated Liaocheng Second People's Hospital, Linqing, Shandong, China (mainland).
DongJian GeDepartment of Anesthesiology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu, China (mainland).
Shanshan WangDepartment of Anesthesiology, Huaiyin Hospital of Huaian City, Huai'an, Jiangsu, China (mainland).
Bin QiDepartment of Anesthesiology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu, China (mainland).
Huaian First People’s Hospital · CNNanjing Medical University · CNTaishan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND The aim of this study was to investigate the protective effect of β-casomorphin-7 (β-CM-7) and its possible mechanisms on acute kidney injury (AKI). MATERIAL AND METHODS Rats were randomly divided into a sham group, a cecal ligation and puncture (CLP) group, and a CLP+β-CM-7 group. Kidney index, kidney function, and histopathology changes were assessed. The expression of neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (Kim-1), nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha (IκBα), and p-IκBα in kidney tissues were detected by Western blotting. Inflammatory and oxidative stress factors were detected by ELISA kits. RESULTS The results showed that treatment with β-CM-7 reduced the levels of creatinine (Cre), blood urea nitrogen (BUN), NGAL, and Kim-1 induced by CLP, weakening the pathological damage. In the CLP + β-CM-7 group, the tumor necrosis factor-α (TNF-α) level and the DNA-binding activity of NF-κB p65 were significantly reduced and the interleukin-10 (IL-10) level was significantly increased compared with the CLP group. β-CM-7 decreased the expression of p-IκBα/IκBα. In addition, β-CM-7 increased the activity of superoxide dismutase (SOD) and decreased the level of malondialdehyde (MDA) in kidney tissue. CONCLUSIONS β-CM-7 attenuated sepsis-induced AKI through reducing inflammation and oxidative stress and by inhibition of nuclear factor (NF)‑κB activities. This study provides a new therapeutic agent for attenuating sepsis-induced kidney injury.

Indexed as

Acute Kidney InjuryAnimalsBlood Urea NitrogenCecumCell Adhesion MoleculesCreatinineEndorphinsInflammationKidneyLigationLipocalin-2MaleMalondialdehydeNF-kappa BNF-KappaB Inhibitor alphaOxidative Stressbeta-casomorphin 7Cell Adhesion MoleculesCreatinineEndorphinsHavcr1 protein, ratLipocalin-2MalondialdehydeNF-kappa BNF-KappaB Inhibitor alphaPeptide Fragments

Identifiers

PMID30610183
PMCPMC6330023
OpenAlexW2907090121

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.