Evidence map›Paper›PMID 38236386›Full record

ArticleInflammation2024

IL-1β Antagonist Receptor Peptide Associated with Photobiomodulation Accelerates Diabetic Wound Tissue Repair.

Rubya Pereira Zaccaron, Laura de Roch Casagrande, Ligia Milanez Venturini, João Vitor Silvano Bittencourt, Camila da Costa, Ellen de Pieri, Anand Thirupathi, Gislaine Tezza Rezin, Ricardo Andrez Machado-de-Ávila, Paulo Cesar Lock Silveira

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
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 3 institutions in 2 countries.

Rubya Pereira ZaccaronLaboratory of Experimental Physiopathology, Program of Postgraduate in Science of Health, Universidade Do Extremo Sul Catarinense, Santa Catarina State, Av. Universitária, 1105 Universitário-Block S, Room 17, Criciúma, 88806-000, Brazil.
Laura de Roch CasagrandeLaboratory of Experimental Physiopathology, Program of Postgraduate in Science of Health, Universidade Do Extremo Sul Catarinense, Santa Catarina State, Av. Universitária, 1105 Universitário-Block S, Room 17, Criciúma, 88806-000, Brazil.
Ligia Milanez VenturiniLaboratory of Experimental Physiopathology, Program of Postgraduate in Science of Health, Universidade Do Extremo Sul Catarinense, Santa Catarina State, Av. Universitária, 1105 Universitário-Block S, Room 17, Criciúma, 88806-000, Brazil.
João Vitor Silvano BittencourtLaboratory of Experimental Physiopathology, Program of Postgraduate in Science of Health, Universidade Do Extremo Sul Catarinense, Santa Catarina State, Av. Universitária, 1105 Universitário-Block S, Room 17, Criciúma, 88806-000, Brazil.
Camila da CostaLaboratory of Experimental Physiopathology, Program of Postgraduate in Science of Health, Universidade Do Extremo Sul Catarinense, Santa Catarina State, Av. Universitária, 1105 Universitário-Block S, Room 17, Criciúma, 88806-000, Brazil.
Ellen de PieriLaboratory of Experimental Physiopathology, Program of Postgraduate in Science of Health, Universidade Do Extremo Sul Catarinense, Santa Catarina State, Av. Universitária, 1105 Universitário-Block S, Room 17, Criciúma, 88806-000, Brazil.
Anand ThirupathiResearch Academy of Medicine Combining Sports, Ningbo No. 2 Hospital, Ningbo, 315099, China.
Gislaine Tezza RezinLaboratory of Neurobiology of Inflammatory and Metabolic Processes, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNISUL), Tubarão, Santa Catarina, Brazil.
Ricardo Andrez Machado-de-ÁvilaLaboratory of Experimental Physiopathology, Program of Postgraduate in Science of Health, Universidade Do Extremo Sul Catarinense, Santa Catarina State, Av. Universitária, 1105 Universitário-Block S, Room 17, Criciúma, 88806-000, Brazil.
Paulo Cesar Lock SilveiraLaboratory of Experimental Physiopathology, Program of Postgraduate in Science of Health, Universidade Do Extremo Sul Catarinense, Santa Catarina State, Av. Universitária, 1105 Universitário-Block S, Room 17, Criciúma, 88806-000, Brazil. psilveira@unesc.net.
Universidade do Extremo Sul Catarinense · BRNingbo No. 2 Hospital · CNUniversidade do Sul de Santa Catarina · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic hyperglycemia caused by diabetes mellitus (DM) slows down the healing process due to prolonged inflammation which impedes the regeneration progression. Photobiomodulation (PBM) is considered a non-pharmacological intervention and has anti-inflammatory and biostimulatory effects that accelerate the healing process. Currently found IL-1β inhibitors are difficult to implement due to their cytotoxic potential, excessive amounts, and invasive administration, and therefore, the application of this peptide in diabetic wounds represents a promising intervention to help resolve the inflammatory response. This study aimed to investigate the effect of an IL-1β inhibitor molecule associated with PBM irradiation in a model of epithelial injury in diabetic mice. After the induction of the DM model with streptozotocin (STZ), the skin lesion model was implemented through surgical excision. Sixty C57BL/6 mice divided into five experimental groups (n = 12) were used: excisional wound (EW), DM + EW, DM + EW + DAP 1-2 (inhibitor peptide), DM + EW + PBM, and DM + EW + PBM + DAP 1-2. Treatment started 12 h after wound induction and was performed daily for 5 days. Twenty-four hours after the last application, the animals were euthanized and the outer edge of the wound was removed. The results obtained demonstrate that the DM + EW + PBM + DAP 1-2 group caused a reduction in the levels of pro-inflammatory cytokines, an increase in anti-inflammatory cytokines, and an increase in TGF-β and maintenance of the cellular redox state with a consequent reduction in levels of inflammatory infiltrate and concomitant stimulation of type III collagen gene expression, as well as a decrease in the size of the wound in square centimeter 6 days after the injury. Only the combination of therapies was able to favor the process of tissue regeneration due to the development of an approach capable of acting at different stages of the regenerative process, through the mechanisms of action of interventions on the inflammatory process by avoiding its stagnation and stimulating progression of regeneration.

Indexed as

Diabetes Mellitus, ExperimentalLow-Level Light TherapyMice, Inbred C57BLWound HealingAnimalsInterleukin-1betaMaleMiceInterleukin-1betadiabetic woundinflammationoxidative stress.peptidephotobiomodulation

Identifiers

PMID38236386
OpenAlexW4390963911

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.