Evidence map›Paper›PMID 42560464›Full record

ArticleSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society2026

Melittin attenuates imiquimod-induced psoriatic dermatitis in mice: a role for autophagy activation via PI3K/Akt/mTOR pathway suppression.

Saeed A Hafez, Asmaa A Ahmed, Abeer Elkhoely, Amany A E Ahmed

Abstract read
In one paragraph

Article in Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

4 authors.

Saeed A HafezHealth Holding Company, Aseer Health Cluster, Saudi Ministry of Health, Abha, Saudi Arabia.
Asmaa A AhmedPharmacology and Toxicology Department, Faculty of Pharmacy, Helwan University, Ein Helwan, Egypt.
Abeer ElkhoelyPharmacology and Toxicology Department, Faculty of Pharmacy, Helwan University, Ein Helwan, Egypt. abir_alkholy@pharm.helwan.edu.eg.
Amany A E AhmedPharmacology and Toxicology Department, Faculty of Pharmacy, Helwan University, Ein Helwan, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite multiple therapeutic strategies, a significant proportion of psoriatic patients fail to achieve complete/sustained disease clearance, highlighting the need for effective adjuvant or alternative therapy. Melittin, the main component in bee venom, exhibits valuable anti-inflammatory and immunomodulatory properties in various diseases; meanwhile, its effect on psoriasis has not been explored yet. Our study aims to investigate the anti-psoriatic effect of melittin with possible involvement of phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) and the autophagy pathways. Mice were divided into 5 groups: Control group, Imiquimod (IMQ) group, and groups (3-5) received daily intraperitoneal injections of methotrexate (MTX, 1 mg/kg), melittin (40 mg/kg), or melittin (80 mg/kg), respectively. All groups except the control received topical IMQ for seven days. Melittin 80 demonstrated superior efficacy, significantly reducing the clinical Psoriasis Area and Severity Index score by 60% and epidermal thickening by 58.55%. Mel 80 decreased malondialdehyde by 62.32%, increased glutathione by 1.44-fold, and reduced nuclear factor-kappa B p65, tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6, IL-23, and IL-17 levels by 72.10%, 83.70%, 61.54%, and 58.09%, 64.55%, and 55.19%, indicating suppression of the pathogenic IL-23/IL-17 axis. Furthermore, Melittin 80 inhibited PI3K/Akt pathway, decreasing p-Akt and PI3K by 50.88% and 57.30%, leading to downregulation of phosphorylated mammalian target of rapamycin (p-mTOR) by 58.53% and a 3.01-fold increase in Beclin-1, indicating restored autophagy. Epidermal proliferation was reduced, with a 58.80% reduction in Epidermal Growth Factor Receptor and 46.51% reduction in Ki67 expression. These results suggest that melittin may represent a promising antioxidant and anti-inflammatory agent for psoriasis, acting through PI3K/Akt/mTOR pathway inhibition and autophagy restoration.

Indexed as

AutophagyImiquimodMelittinmTORPI3K/AktPsoriasis

Identifiers

PMID42560464
PMCPMC13447632

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.