Evidence map›Paper›PMID 38832986›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2024

Tanshinol ameliorates imiquimod-induced psoriasis by inhibiting M1 macrophage polarization through suppression of the notch signaling pathway.

Junhao Liu, Shuangshuang Yong, Sisi Yin, Jinhong Feng, Caihua Lian, Jie Chen

Abstract read
In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–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

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. A review of core immuno-inflammatory mechanisms and key regulatory targets in psoriasis.American journal of clinical and experimental immunology · 2026
    Review
4 · The record

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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

6 authors.

Junhao LiuDepartment of Dermatology, Tongchuan distric people's hospital of dazhou, Dazhou, China.
Shuangshuang YongDepartment of Dermatology, Dachuan distric people's hospital of dazhou, Dazhou, China.
Sisi YinDepartment of Medical Aesthetics, Affiliated Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Jinhong FengDepartment of Medical Aesthetics, Affiliated Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Caihua LianDepartment of Dermatology, Chengdu Seventh People's Hospital (Affiliated Cancer Hospital of Chengdu Medical College), Chengdu, China.
Jie ChenDepartment of Dermatology, Gulin Traditional Chinese Medicine Hospital, Luzhou, China. cj208208@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPsoriasis is a common immune-related chronic inflammatory skin disease, often accompanied by significant itching, and once diseased, the course of the disease lasts for most of the lifetime. Tanshinol (TAN) is an active ingredient of Salvia miltiorrhiza, which possesses pharmacological effects such as anti-inflammatory and antioxidant properties. However, the effects of TAN on psoriasis have not been widely reported. Therefore, the aim of this study was to investigate the therapeutic effects and mechanisms of TAN in psoriasis.

methodsAn imiquimod (IMQ)-induced psoriasis mouse model was constructed and treated with different doses of TAN to observe the changes in skin lesion phenotype, macrophage polarization, inflammation and Notch signaling pathway in mice. Further removal of macrophages or inhibition or activation of Notch signaling pathway was performed to examine the changes in skin lesion phenotype, macrophage polarization, inflammation and Notch signaling pathway in mice. In addition, in vitro experiments verified that TAN regulates RAW264.7 macrophage polarization and cytokine secretion through the Notch pathway.

resultsThe results showed that TAN alleviated IMQ-induced skin lesions and pathological phenotypes in psoriasis mice and inhibited Notch signaling pathway and M1-type macrophage polarization. Moreover, macrophage clearance and Notch signaling pathway activation inhibited the effect of TAN on psoriasis. Further in vitro experiments showed that Notch agonists reversed the effects of TAN on macrophage polarization and inflammatory cytokines.

conclusionsCollectively, these findings suggest that TAN may exert a therapeutic effect on psoriasis by inhibiting the Notch signaling pathway and thus M1-type macrophage polarization.

Indexed as

ImiquimodMacrophagesPsoriasisReceptors, NotchSignal TransductionAnimalsAnti-Inflammatory AgentsCaffeic AcidsCytokinesDisease Models, AnimalMaleMiceMice, Inbred BALB CMice, Inbred C57BLRAW 264.7 CellsSkinAnti-Inflammatory AgentsCaffeic AcidsCytokinesImiquimodReceptors, NotchtanshinolMacrophages polarizationNotch signaling pathwayPsoriasisTanshinol

Identifiers

PMID38832986
PMCPMC11522191

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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.