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. 2022 Apr 14:2022:3193572.
doi: 10.1155/2022/3193572. eCollection 2022.

Intervention Mechanism of Hunag-Lian Jie-Du Decoction on Canonical Wnt/ β-Catenin Signaling Pathway in Psoriasis Mouse Model

Xuesong Yang  1 , Guangyun Luo  2 , Lan Fu  3 , Hong Huang  1 , Lifen Wang  1 , Lihua Yin  4 , Xuelian Zhang  1 , Tingting Wang  1 , Xuan Ma  1 , Tianyu Feng  1 , Jianzhou Ye  1
Affiliations

Intervention Mechanism of Hunag-Lian Jie-Du Decoction on Canonical Wnt/ β-Catenin Signaling Pathway in Psoriasis Mouse Model

Xuesong Yang et al. Evid Based Complement Alternat Med. .

Abstract

Background: Psoriasis is a common chronic inflammatory skin disease with multifactor etiology, characterized by abnormal proliferation and differentiation of keratinocytes. Huang-Lian Jie-Du decoction (HLJDD) is a traditional Chinese medicine prescription with good clinical curative effect on psoriasis. However, its therapeutic mechanisms are still unclear.

Methods: The psoriasis model of SKH-1 nude mice was established by imiquimod-induced and HLJDD gavage was given. Hematoxylin and eosin staining were used to evaluate pathological morphologies, and immunohistochemistry was used to detect the expressions of Wnt1, β-catenin, and c-Myc in psoriasis mice. Western blot was used to examine the expressions of Frizzled-2, LRP5/6, GSK-3β, APC, Axin2, TCF4, LEF1, cyclin D1, TBX3, EPHB2, and NOTUM enzyme.

Results: In this study, HLJDD reduced skin erythema and lesions, decreased the thickness of epidermal and downregulated the expressions of Wnt1, β-catenin, and c-Myc. Western blot results showed that HLJDD reduced the expressions of Wnt receptors Frizzled-2 and LRP5/6, and Wnt downstream target genes TCF4, LEF1, cyclin D1, TBX3, and EPHB2, while upregulated destruction complex proteins GSK-3β, APC, and Axin2.

Conclusions: HLJDD can effectively treat psoriasis and inhibit the Wnt/β-catenin signaling pathway at multiple stages.

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Conflict of interest statement

The authors declare that they have no conflicts of interest.

Figures

Figure 1
Figure 1
The effect of HLJDD treatment in psoriasis mouse. (a) Workflow of the study. (b) Images of phenotypical presentation of mouse back skin on day 6 and day 14. (c) H&E staining of the back skin of mice (magnification 10× and 40×).
Figure 2
Figure 2
HJLDD reduced Wnt1, β-catenin, and c-Myc in psoriasis mouse. (a) Representative IHC staining of Wnt1, β-catenin, and c-Myc in section of mouse skin samples. Scale bars, 500 μm. (b) Percentage of Wnt1-, β-catenin-, and c-Myc-positive cells in psoriasis mouse skin samples. Data are presented as the mean ± SD of three independent experiments performed in triplicate. ∗P < 0.0001 vs. control group; #P < 0.0001 vs. IMQ group.
Figure 3
Figure 3
The expression of Wnt receptors and DCs in back skin sample of psoriatic mice. (a) Western blot of Frizzled-2, LRP6, and LRP5 protein levels in skin samples of psoriasis mice. (b) Western blot of GSK-3β, APC, and Axin2 protein levels in skin samples of psoriasis mice. Data are presented as the mean ± SD of three independent experiments performed in triplicate. ∗P < 0.0001 vs. control group; #P < 0.0001 vs. IMQ group.
Figure 4
Figure 4
The effect of HLJDD on Wnt target genes in psoriatic mice. (a, b) Western blot of TCF4, LEF1, cyclin D1, TBX3, EPHB2, and NOTUM protein levels in skin samples of psoriasis mice. (c) A comparison of TCF4, LEF1, cyclin D1, TBX3, EPHB2, and NOTUM protein expression levels in skin samples of psoriasis mice. Data are presented as the mean ± SD of three independent experiments performed in triplicate. ∗P < 0.0001 vs. control group; #P < 0.0001 vs. IMQ group.
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References

    1. Rendon A., Schäkel K. Psoriasis pathogenesis and treatment. International Journal of Molecular Sciences . 2019;20(6) doi: 10.3390/ijms20061475. - DOI - PMC - PubMed
    1. Bocheńska K., Smolińska E., Moskot M., Jakóbkiewicz-Banecka J., Gabig-Cimińska M. Models in the research process of psoriasis. International Journal of Molecular Sciences . 2017;18(12) doi: 10.3390/ijms18122514. - DOI - PMC - PubMed
    1. Xue Y., Liu Y., Bian X., et al. miR‐205‐5p inhibits psoriasis‐associated proliferation and angiogenesis: Wnt/β‐catenin and mitogen‐activated protein kinase signaling pathway are involved. The Journal of Dermatology . 2020;47(8):882–892. doi: 10.1111/1346-8138.15370. - DOI - PubMed
    1. Langley R. G., Krueger G. G., Griffiths C. E. Psoriasis: epidemiology, clinical features, and quality of life. Annals of the Rheumatic Diseases . 2005;64:18–23. doi: 10.1136/ard.2004.033217. - DOI - PMC - PubMed
    1. Stern R. S. Psoriasis. The Lancet . 1997;350(9074):349–353. doi: 10.1016/s0140-6736(97)05257-4. - DOI - PubMed