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Momordin Ic ameliorates psoriasis skin damage in mice via the IL-23/IL-17 axis

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Abstract

Psoriasis, a chronic and easily recurring inflammatory skin disease, causes a great economic burden to the patient’s family because the etiology and mechanism are still unclear and the treatment cycle is long. In this study, the function and related mechanisms of Momordin Ic in psoriasis were investigated. The IMQ-induced mouse psoriasis model was constructed. The protective effects of different doses of Momordin Ic on psoriasis skin damage in mice were detected by PASI score, HE staining and Ki-67 staining. A psoriasis-like keratinocyte model was established at the cellular level using M5 (IL-17A, IL-22, oncostatin M, IL-1α, and TNF-α) triggered HaCaT. The effects of Momordin Ic upon HaCaT cell biological behavior were examined using MTT and CCK-8 assays. In terms of mechanism, the expression level of each inflammatory factor was assessed using IHC staining and/or ELISA, qRT-PCR, the expression of oxidative stress-related indicators was detected biochemically, and western blot was performed to detect the levels of key proteins of the Wnt signaling and VEGF. As the results shown,  at the in vivo level, Momordin Ic significantly alleviated skin damage, reduced PASI score and inhibited hyperproliferation of keratinized cells in psoriasis mice. At the cellular level, Momordin Ic also significantly reversed M5-induced hyperproliferation of HaCaT keratinocytes. In terms of mechanism, Momordin Ic significantly inhibited the IL-23/IL-17 axis, dramatically elevated the levels of intracellular antioxidants including SOD, GSH-Px, and CAT, and significantly down-regulated the levels of the indicator of oxidative damage, malondialdehyde (MDA). In addition, Momordin Ic also significantly inhibited the level of β-catenin, a pivotal protein of the Wnt signaling, C-Myc, a target gene of the Wnt signaling, and VEGF, a critical protein of angiogenesis. In conclusion, Momordin Ic can be involved in the skin-protective effects of psoriasis by multiple mechanisms, including inhibition of the Wnt signaling pathway and the IL-23/IL-17 axis, and suppression of oxidative damageand VEGF expression. Momordin Ic has been proven to be an underlying therapeutic drug for the treatment of psoriasis.

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Funding

This study was supported by the National Natural Science Foundation of China (No. 82174378).

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Author notes

  1. Chang Wang and Simin Jiao contributed equally to this work.

Authors and Affiliations

  1. Department of Dermatology, the Second Affiliated Hospital, The Domestic First-Class Discipline Construction Project of Chinese Medicine, Hunan University of Chinese Medicine, Changsha, 410005, Hunan, China

    Chang Wang, Simin Jiao, Rong Zhou, Pan Huang, Bijun Zeng, Zhibo Yang & Junwen Wang

Authors
  1. Chang Wang
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  2. Simin Jiao
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  3. Rong Zhou
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  4. Pan Huang
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  7. Junwen Wang
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Contributions

C,W and SM,J performed the experiments and wrote the main manuscript text and performed the experiments. R,Z and P,H coordinated the study and assisted with the experiments. BJ,Z and ZB,Y guided the experiment and plan. JW,W. conceived the study, designed the experiments, and revised the paper. All the authors have reviewed and approved the manuscript.

Corresponding author

Correspondence to Junwen Wang.

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The authors declare no competing interests.

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All procedures performed were in accordance with the ethical standards granted by the Second Affiliated Hospital of Hunan University of Chinese Medicine Animal Experiment Center.

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The data supporting this study’s findings are available from the corresponding author upon reasonable request.

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Wang, C., Jiao, S., Zhou, R. et al. Momordin Ic ameliorates psoriasis skin damage in mice via the IL-23/IL-17 axis. Arch Dermatol Res 316, 474 (2024). https://doi.org/10.1007/s00403-024-03023-y

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  • DOI: https://doi.org/10.1007/s00403-024-03023-y

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