Huanglian ointment alleviates eczema by maintaining the balance of c-Jun and JunB and inhibiting AGE-RAGE-mediated pro-inflammation signaling pathway

Wang, Siming; Wang, Yuanxi; Han, Bing; Chen, Yanyan; Bai, Xueyuan; Yu, Shiting; Liu, Meichen

doi:10.1016/j.phymed.2022.154372

Cited by 11 publications

(9 citation statements)

References 53 publications

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“…Coptis chinensis has been widely used as a topical agent for skin disease, including eczema, 27 rosacea, 28 SUV‐induced dermatitis and psoriasis 29 . Worenine, extracted from the dried rhizome of Coptis chinensis , was found to prevent SUV‐induced sunburn in our previous study.…”

Section: Discussionmentioning

confidence: 87%

TOPK promotes the development of psoriasis and worenine alleviates psoriasiform dermatitis by inhibiting TOPK activity

Lu,

Huang,

et al. 2023

Acad Dermatol Venereol

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BackgroundPsoriasis is an inflammatory skin disease. The pathogenesis of psoriasis has not been fully elucidated. T‐lymphokine‐activated killer cell‐originated protein kinase (TOPK) activity increases in a proinflammatory environment, and inhibiting TOPK blocks inflammation. However, whether TOPK is involved in the pathogenesis of psoriasis remains to be identified.ObjectivesWe aimed to study the role of TOPK in psoriasis and attempted to find a drug targeting TOPK for the prevention and treatment of psoriasis.MethodFirstly, the expressions of TOPK in psoriatic patients, psoriatic cell and animal model were analysed by Gene Expression Omnibus database, immunohistochemistry (IHC) staining and western blot (WB). After inhibiting TOPK by chemical or gene knockout, the effect of TOPK on the development of psoriasis was verified in cell and animal model by WB, qRT‐PCR, ELISA, haematoxylin–eosin (H&E) and IHC staining. Moreover, phosphoproteomic analysis was performed to explore the signalling pathways regulated by TOPK in the occurrence and development of psoriasis. Then, an in vitro kinase assay was performed to prove TOPK kinase activity was inhibited by worenine. Ultimately, WB, qRT‐PCR, ELISA, H&E and IHC staining were used to verify the anti‐psoriasis effect of worenine by inhibiting TOPK was in cell and animal model.ResultsIn this study, we found that TOPK was highly expressed in psoriasis patients, psoriatic cell and animal model, which suggests that TOPK might be associated with psoriasis pathogenesis. Interestingly, chemical or genetic inhibition of TOPK alleviated M5‐ and imiquimod (IMQ)‐induced psoriasis‐like dermatitis, which further confirmed the role of TOPK in promoting the development of psoriasis. Moreover, we determined that worenine inhibited TOPK kinase activity. In addition, worenine relieved M5‐ and IMQ‐induced psoriasiform dermatitis by inhibiting TOPK activity.ConclusionsT‐lymphokine‐activated killer cell‐originated protein kinase promotes the development of psoriasis. Therefore, TOPK might be a promising drug target for the prevention and treatment of psoriasis. Worenine alleviates psoriasiform dermatitis by inhibiting TOPK activity, providing new strategies for clinical intervention.

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Section: Discussionmentioning

confidence: 87%

TOPK promotes the development of psoriasis and worenine alleviates psoriasiform dermatitis by inhibiting TOPK activity

Lu,

Huang,

et al. 2023

Acad Dermatol Venereol

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“…5), the AGE-RAGE signaling pathway was signi cantly enriched. There is evidence that advanced glycation end products (AGEs) are the products of excessive sugar and protein binding, which interact with the AGE receptor (RAGE) and activate downstream factor nuclear factor-kappaB (NF-κB) through the AGE-RAGE signaling pathway, thereby promoting the in ammatory response [13]. These ndings suggest that the most prominent feature of early fracture healing is a highly in ammatory response.…”

Section: Discussionmentioning

confidence: 99%

The whole transcriptomic analysis of local bone tissue after fracture

Wang,

Guo,

Yuan

et al. 2024

Preprint

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Fracture healing is a complex physiological process involving multiple cells and signaling pathways, the potential molecular mechanisms and biological process are still unclear and need further exploration. In this study, transcriptome sequencing technology was used to detect and analyze the changes in transcriptome of the local injury tissue after fracture. Differentially expressed genes (DEGs) with the high degree were analyzed. Our results showed that different stages of fracture healing had different focuses, some important biological processes, such as the inflammatory response, mainly occurred on the 3rd day after fracture. Besides, we found that the 3rd day after fracture was a key point of transcriptome change, and neural regulation played a significant role in fracture healing at this time, and inflammatory stimulation might be an important factor affecting neural regulation after fracture. In conclusion, our research results identify some important genes and pathways in the process of fracture healing, and summarize the main characteristics of transcriptome changes in fractures. This laid the foundation for a deeper understanding of the relation between molecular mechanisms and biological processes involved in fracture healing. By identifying the specific time points at which various cellular events occur during the healing process, researchers can gain insights into the complex interplay between cells, signaling pathways, and extracellular matrix components that is required for successful bone healing. This knowledge can inform the development of new therapies and interventions to improve fracture healing outcomes and ultimately enhance the quality of life for patients affected by bone fractures.

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“…IVL is a protein component of human skin. It is a structural protein precursor of the keratinocyte-cornified envelope, a protective sheath of covalently crosslinked proteins that is formed during the final stages of keratinocyte differentiation [ 33 ]. In this study, compound 1 upregulated IVL expression but failed to upregulate the FLG expression, which was decreased by TNF-α and IFN-γ treatment.…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Effects Exerted by 14-Methoxyalternate C from Antarctic Fungal Strain Pleosporales sp. SF-7343 via the Regulation of NF-κB and JAK2/STAT3 in HaCaT Human Keratinocytes

Dong

Cao

Liu

et al. 2022

IJMS

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Atopic dermatitis (AD) is a chronic inflammatory skin disease with a profound negative impact on patients’ quality of life. Four known secondary fungal metabolites were found in the chemical study of the Antarctic fungus Pleosporales sp. SF-7343, including 14-methoxyalternate C (1), 5′-methoxy-6-methyl-biphenyl-3,4,3′-triol (2), 3,8,10-trihydroxy-4-methoxy-6-methylbenzocoumarin (3), and alternariol monomethyl ether (4). Additionally, we identified the skin anti-inflammatory composition from the SF-7343 strain. Interleukin-8 and -6 Screening results showed that compound 1 inhibited IL-8 and IL-6 in tumor necrosis factor-α/interferon-γ stimulated HaCaT cells. Compound 1 showed inhibitory effects on MDC and RANTES. It also downregulated the expression of intercellular adhesion molecule-1 (ICAM-1) and upregulated the expression of involucrin. The results of the mechanistic study showed that compound 1 inhibited the nuclear translocation of nuclear factor-kappa B p65 and STAT3. In conclusion, this study demonstrates the potential of the Antarctic fungal strain SF-7343 as a bioactive resource to inhibit skin inflammation, such as AD.

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Huanglian ointment alleviates eczema by maintaining the balance of c-Jun and JunB and inhibiting AGE-RAGE-mediated pro-inflammation signaling pathway

Cited by 11 publications

References 53 publications

TOPK promotes the development of psoriasis and worenine alleviates psoriasiform dermatitis by inhibiting TOPK activity

TOPK promotes the development of psoriasis and worenine alleviates psoriasiform dermatitis by inhibiting TOPK activity

The whole transcriptomic analysis of local bone tissue after fracture

Anti-Inflammatory Effects Exerted by 14-Methoxyalternate C from Antarctic Fungal Strain Pleosporales sp. SF-7343 via the Regulation of NF-κB and JAK2/STAT3 in HaCaT Human Keratinocytes

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