Evidence map›Paper›PMID 41836725›Full record

ArticleInternational journal of nanomedicine2026

Enhancement of Psoriasis Treatment by Phellodendri Chinensis Cortex Carbon Dots (PCC-CDs) Through Modulation of the HMGB1/TLR4/MAPK/NF-κB Pathway.

Xinrong Tian, Hui Kong, Shuxian Wang, Xiwen Zhang, Chenxin He, Yan Huang, Ruiyan Liu, Ertong Dai, Guojiao Shang, Yue Zhang and 4 more

Abstract read
In one paragraph

Article in International journal of nanomedicine, 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

14 authors.

Xinrong Tian *School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Hui Kong *School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, People's Republic of China.ORCID 0000-0002-1382-7985
Shuxian WangSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Xiwen ZhangSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Chenxin HeSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Yan HuangSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Ruiyan LiuSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Ertong DaiSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Guojiao ShangSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, People's Republic of China.ORCID 0009-0006-7636-7564
Yue ZhangSchool of Life Sciences, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Cheng JinjunSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Zhanxue SunDepartment of Dermatology and Venereology, Beijing University of Chinese Medicine Third Affiliated Hospital, Beijing, People's Republic of China.ORCID 0009-0002-1357-4508
Huihua QuCenter of Scientific Experiment, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Yan ZhaoSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Psoriasis is a chronic, debilitating inflammatory skin disorder mediated by the immune system. It is characterized by excessive keratinocyte proliferation and abnormal differentiation, leading to symptoms that significantly impair the quality of life of affected individuals. Despite extensive research, no effective drugs are currently available to completely inhibit the progression of psoriasis. Purpose: This study aims to explore the therapeutic potential and underlying mechanisms of Phellodendron chinense charcoal carbon dots (PCC-CDs) in treating psoriasis. PCC-CDs have recently garnered attention due to their sustained anti-inflammatory properties and unique bioavailability. Methods: This study explores the therapeutic potential and underlying mechanisms of PCC-CDs in psoriasis treatment via detailed pharmacological experiments in an imiquimod (IMQ)-induced mouse model, including topical PCC-CDs application, inflammatory mediator detection, histopathological assessment of tissue damage, and transcriptomic as well as molecular biology analyses focusing on the modulation of the HMGB1/TLR4 and MAPK/NF-κB inflammatory signaling pathways. Results: In the IMQ-induced mouse model, PCC-CDs effectively suppressed the levels of inflammatory mediators and reduced histopathological damage. Molecular analyses revealed that PCC-CDs may exert their therapeutic effects by modulating the inflammatory response mediated by the HMGB1/TLR4 pathway, primarily through inhibiting protein expression in the MAPK/NF-κB signaling cascade. The application of PCC-CDs resulted in a significant reduction in psoriasis-like symptoms in IMQ-induced mice, including marked improvements in erythema, scaling, and pruritus. Conclusion: PCC-CDs offer a promising new approach to the clinical management of psoriasis. Their ability to provide sustained anti-inflammatory effects and distinctive bioavailability makes them a potential candidate for further development as a therapeutic agent. This study highlights the importance of PCC-CDs in modulating key inflammatory pathways, offering hope for improved treatment options for individuals suffering from psoriasis.

Indexed as

Anti-Inflammatory AgentsCarbon Quantum DotsPhellodendronPsoriasisAnimalsCharcoalDisease Models, AnimalHMGB1 ProteinHumansImiquimodMaleMiceNF-kappa BSignal TransductionToll-Like Receptor 4Anti-Inflammatory AgentsCharcoalHMGB1 ProteinImiquimodNF-kappa BTlr4 protein, mouseToll-Like Receptor 4HMGB1inflammatory responsepharmacological mechanismsphellodendron chinense charcoal carbon dots spraypsoriasis

Identifiers

PMID41836725
PMCPMC12988753

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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.