Evidence map›Paper›PMID 33488946›Full record

ArticleOxidative medicine and cellular longevity2021

Melittin Ameliorates Endotoxin-Induced Acute Kidney Injury by Inhibiting Inflammation, Oxidative Stress, and Cell Death in Mice.

Jung-Yeon Kim, Jaechan Leem, Hyo-Lim Hong

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  3. Therapeutic Bioactivity Exerted by theMolecules (Basel, Switzerland) · 2025
    Article
  4. Melittin inhibits MPPThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
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  14. Cordycepin- melittin nanoconjugate intensifies wound healing efficacy in diabetic rats.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
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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

3 authors at 1 institution in 1 country.

Jung-Yeon KimDepartment of Immunology, School of Medicine, Catholic University of Daegu, Daegu 42472, Republic of Korea.ORCID https://orcid.org/0000-0001-7229-1466
Jaechan LeemDepartment of Immunology, School of Medicine, Catholic University of Daegu, Daegu 42472, Republic of Korea.ORCID https://orcid.org/0000-0003-2329-4374
Hyo-Lim HongDepartment of Internal Medicine, School of Medicine, Catholic University of Daegu, Daegu 42472, Republic of Korea.ORCID https://orcid.org/0000-0003-2147-1381
Daegu Catholic University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis-related acute kidney injury (AKI) is a worldwide health problem, and its pathogenesis involves multiple pathways. Lipopolysaccharide (LPS) is an endotoxin that induces systemic inflammatory responses. Melittin, a main constituent of bee venom, exerts several biological activities such as antioxidant, anti-inflammatory, and antiapoptotic actions. However, whether melittin protects against endotoxin-induced AKI remains undetermined. Here, we aimed to examine the potential action of melittin on LPS-induced renal injury and explore the mechanisms. We showed that acute renal failure and structural damage after injection of LPS were markedly attenuated by administration of melittin. The peptide also suppressed expression of markers of direct tubular damage in kidneys of the LPS-treated mice. Mechanistically, melittin reduced systemic and renal levels of cytokines and inhibited renal accumulation of immune cells with concomitant suppression of nuclear factor kappa-B pathway. Increased amounts of lipid peroxidation products after LPS treatment were largely decreased by melittin. Additionally, the peptide decreased expression of nicotinamide adenine dinucleotide phosphate oxidase 4 and enhanced nuclear factor erythroid-2-related factor 2-mediated antioxidant defenses. Moreover, melittin inhibited apoptotic and necroptotic cell death after LPS treatment. Lastly, we showed that melittin improved the survival rate of LPS-injected mice. These results suggest that melittin ameliorates endotoxin-induced AKI and mortality through inhibiting inflammation, oxidative injury, and apoptotic and necroptotic death of tubular epithelial cells.

Indexed as

ApoptosisOxidative StressAcute Kidney InjuryAnimalsAnti-Inflammatory AgentsAntioxidantsCell DeathEndotoxinsInflammationMaleMelittenMiceMice, Inbred C57BLProtective AgentsAnti-Inflammatory AgentsAntioxidantsEndotoxinsMelittenProtective Agents

Identifiers

PMID33488946
PMCPMC7803412
OpenAlexW3118635961

What OpenQuestion holds

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LicenceCC BY
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.