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当归饮子通过皮肤修复、抗氧化和平衡外周μ-阿片受体减轻瘙痒相关性特应性皮炎。

Angelica Yinzi Alleviates Pruritus-Related Atopic Dermatitis through Skin Repair, Antioxidation, and Balancing Peripheral - and -opioid Receptors.

作者信息

Liu Wei, Luo Yang, Song Wanci, Dan Hanxiong, Li Li, Zhou Daonian, You Pengtao

机构信息

Beijing Key Laboratory of Molecular Pharmaceutics and New Drug Delivery Systems, School of Pharmaceutical Sciences, Peking University, Beijing 100191, China.

Research Center, Mayinglong Pharmaceutical Group Co. Ltd., Wuhan 430060, Hubei, China.

出版信息

Evid Based Complement Alternat Med. 2023 Sep 25;2023:6058951. doi: 10.1155/2023/6058951. eCollection 2023.

DOI:10.1155/2023/6058951
PMID:37790739
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10545464/
Abstract

BACKGROUND

Angelica Yinzi (AYZ) is a Chinese traditional herbal formula reported to attenuate itches and inflammation caused by atopic dermatitis (AD). However, the underlying mechanism of AYZ in the attenuation of itchiness and inflammation remains unknown.

OBJECTIVE

This study investigated the mechanism of AYZ in reducing itchiness in mice with 1-chloro-2,4-dinitrobenzene- (DNCB-)-induced atopic dermatitis.

METHODS

Hematoxylin and eosin (H&E) and toluidine blue staining were used to evaluate pathological changes in skin tissue, while an enzyme-linked immunosorbent assay (ELISA) was used to assess the cytokine levels in the skin. After that, qRT-PCR was performed to determine the mRNA levels of cytokines in the skin. Immunofluorescence and western blotting analysis were further used to assess -opioid receptor (MOR) expression and immunohistochemistry to assess the p-ERK, p-AKT, and -opioid receptor (KOR).

RESULTS

The AYZ treatment alleviated the AD clinical symptoms, including decreasing the scratching frequency, the ear thickness, and the infiltration of mast cells, lymphocytes, inflammatory cells, and mononuclear cells. In addition, AYZ inhibited the expression of interleukin (IL)-13, thymic stromal lymphopoietin (TSLP), and reduced neuraminidase (NA), corticotropin-releasing factor (CRF), and reactive oxygen species (ROS) expression. Markers involved in itches, such as p-ERK and p-AKT, were significantly downregulated following AYZ treatment. Besides, AYZ significantly increased MOR expression and downregulated KOR in the epidermis and spinal cord.

CONCLUSION

Our findings imply that AYZ ameliorates pruritus-related AD through skin repair, antioxidation, and balancing peripheral MOR and KOR. The findings in this study lay a theoretical foundation for the control mechanism of peripheral itch.

摘要

背景

当归饮子是一种据报道可减轻特应性皮炎(AD)引起的瘙痒和炎症的中药复方。然而,当归饮子减轻瘙痒和炎症的潜在机制尚不清楚。

目的

本研究探讨当归饮子减轻1-氯-2,4-二硝基苯(DNCB)诱导的特应性皮炎小鼠瘙痒的机制。

方法

采用苏木精-伊红(H&E)染色和甲苯胺蓝染色评估皮肤组织的病理变化,同时采用酶联免疫吸附测定(ELISA)评估皮肤中的细胞因子水平。之后,进行qRT-PCR以确定皮肤中细胞因子的mRNA水平。进一步采用免疫荧光和蛋白质印迹分析评估μ-阿片受体(MOR)的表达,并采用免疫组织化学评估p-ERK、p-AKT和κ-阿片受体(KOR)。

结果

当归饮子治疗减轻了AD的临床症状,包括降低搔抓频率、耳部厚度以及肥大细胞、淋巴细胞、炎性细胞和单核细胞的浸润。此外,当归饮子抑制白细胞介素(IL)-13、胸腺基质淋巴细胞生成素(TSLP)的表达,并降低神经氨酸酶(NA)、促肾上腺皮质激素释放因子(CRF)和活性氧(ROS)的表达。当归饮子治疗后,与瘙痒相关的标志物如p-ERK和p-AKT显著下调。此外,当归饮子显著增加表皮和脊髓中MOR的表达并下调KOR。

结论

我们的研究结果表明,当归饮子通过皮肤修复、抗氧化以及平衡外周MOR和KOR来改善与瘙痒相关的AD。本研究结果为外周瘙痒的控制机制奠定了理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe59/10545464/550ee163ea4a/ECAM2023-6058951.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe59/10545464/957d3ce2940f/ECAM2023-6058951.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe59/10545464/b50df4380232/ECAM2023-6058951.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe59/10545464/105091d79b39/ECAM2023-6058951.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe59/10545464/91cf55dd0fa9/ECAM2023-6058951.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe59/10545464/f46b3fbc04d8/ECAM2023-6058951.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe59/10545464/550ee163ea4a/ECAM2023-6058951.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe59/10545464/957d3ce2940f/ECAM2023-6058951.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe59/10545464/b50df4380232/ECAM2023-6058951.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe59/10545464/105091d79b39/ECAM2023-6058951.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe59/10545464/91cf55dd0fa9/ECAM2023-6058951.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe59/10545464/f46b3fbc04d8/ECAM2023-6058951.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe59/10545464/550ee163ea4a/ECAM2023-6058951.006.jpg

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