Cordycepin Improves Psoriasis by Balancing Key Skin Cell Proteins

Jenn Hoskins
25th June, 2024

Cordycepin Improves Psoriasis by Balancing Key Skin Cell Proteins

Image Source: Natural Science News, 2024

Key Findings

  • Researchers at Tongji University found that cordycepin, from Cordyceps militaris, can help treat psoriasis
  • Cordycepin inhibits the excessive growth of skin cells by activating the p53 apoptotic pathway
  • In mice with psoriasis-like skin, cordycepin gel reduced inflammation and scaling, showing significant improvement
Psoriasis is a chronic skin condition characterized by the rapid proliferation of keratinocytes, leading to the formation of thick, scaly plaques on the skin. This condition affects millions worldwide, causing both physical discomfort and emotional distress. The primary drivers of psoriasis include genetic predisposition, immune system dysregulation, and environmental factors[2][3]. Recent advances have highlighted the central role of the IL-23/IL-17 axis in the pathogenesis of psoriasis, leading to new therapeutic approaches targeting these cytokines[2]. However, the quest for effective and affordable treatments continues. A recent study conducted by researchers at Tongji University has explored the potential of cordycepin, a compound derived from Cordyceps militaris, in treating psoriasis[1]. This study provides new insights into the mechanism by which cordycepin exerts its effects, particularly focusing on the p53 apoptotic pathway. Apoptosis, or programmed cell death, is a crucial process for maintaining cellular homeostasis and immune system function. Dysregulation of apoptosis can contribute to various diseases, including psoriasis. In psoriasis, keratinocytes (the predominant cells in the outer layer of the skin) exhibit impaired apoptosis, leading to their excessive proliferation. This study aimed to elucidate how cordycepin influences apoptosis in keratinocytes and its overall effect on psoriasis. The researchers employed bioinformatics analysis to predict that cordycepin might act through the p53 apoptotic pathway. The p53 protein is a well-known tumor suppressor involved in regulating cell cycle and apoptosis. In psoriasis, the p53 pathway is often disrupted, contributing to abnormal keratinocyte proliferation. The study confirmed that cordycepin inhibits the proliferation of HaCaT cells (a human keratinocyte cell line) induced by IL-17A, a cytokine known to play a key role in psoriasis pathogenesis[2]. Additionally, cordycepin down-regulated the expression of proliferating cell nuclear antigen (PCNA) and Ki-67, markers associated with cell proliferation. Further experiments revealed that cordycepin promotes apoptosis by modulating the expression of apoptotic proteins. Specifically, cordycepin increased the levels of BAX (a pro-apoptotic protein) and p53 while decreasing the levels of Bcl-2 (an anti-apoptotic protein). This regulation of apoptotic proteins helps restore the balance between cell proliferation and cell death, which is disrupted in psoriasis. One of the significant findings of the study was the normalization of the abnormal p53-mouse double minute 2 (MDM2) feedback loop by cordycepin. MDM2 is a negative regulator of p53, and their interaction forms a feedback loop that is often disrupted in cancer and other proliferative diseases. By normalizing this loop, cordycepin helps re-establish the proper function of the p53 pathway, promoting apoptosis and reducing keratinocyte proliferation. In addition to in vitro experiments, the researchers tested the efficacy of cordycepin in an in vivo model. Mice with imiquimod (IMQ)-induced psoriasis-like skin lesions were treated with a cordycepin gel. The results showed significant improvement in the skin lesions, with reduced inflammation and scaling. This effect was accompanied by the normalization of the p53-MDM2 pathway at the protein level, further supporting the role of cordycepin in modulating apoptosis and keratinocyte proliferation. The findings from this study align with previous research on the role of apoptosis in psoriasis and the potential of targeting specific pathways for treatment. For instance, diosgenin, another compound studied for its anti-psoriatic properties, has been shown to inhibit keratinocyte proliferation and promote apoptosis through different mechanisms, including NFκB inhibition and TLR4/Myd88 pathway modulation[4]. Both studies highlight the importance of regulating keratinocyte proliferation and apoptosis in managing psoriasis. In conclusion, the study from Tongji University provides compelling evidence that cordycepin can be developed as an Active Pharmaceutical Ingredient (API) for psoriasis treatment. By targeting the p53 apoptotic pathway, cordycepin helps restore the balance between cell proliferation and cell death, offering a promising approach to managing this chronic skin condition. These findings contribute to the ongoing efforts to develop more effective and affordable treatments for psoriasis, expanding the therapeutic options available to patients.

MedicineHealthBiochem

References

Main Study

1) Cordycepin Ameliorates Psoriasis-Like Skin Lesion by Regulating p53/MDM2 Feedback Loop.

Published 24th June, 2024

https://doi.org/10.1007/s12033-024-01211-9

Related Studies

2) Psoriasis pathogenesis and the development of novel targeted immune therapies.

https://doi.org/10.1016/j.jaci.2017.07.004

3) The current landscape of psoriasis genetics in 2020.

https://doi.org/10.1016/j.jdermsci.2020.05.008

4) The potential of Diosgenin in treating psoriasis: Studies from HaCaT keratinocytes and imiquimod-induced murine model.

https://doi.org/10.1016/j.lfs.2019.117115


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