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大麻二酚的体内外抗炎作用通过JAK/STAT/NFκB信号通路介导。

Anti-Inflammatory Effects of Cannabigerol In Vitro and In Vivo Are Mediated Through the JAK/STAT/NFκB Signaling Pathway.

作者信息

Jeong Ga Hee, Kim Ki Chan, Lee Ji Hyun

机构信息

Department of Medical Sciences, Graduate School of The Catholic University of Korea, Seoul, #222 Banpo-daero, Seocho-gu, Seoul 06591, Republic of Korea.

Department of Dermatology, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, #222 Banpo-daero, Seocho-gu, Seoul 06591, Republic of Korea.

出版信息

Cells. 2025 Jan 9;14(2):83. doi: 10.3390/cells14020083.

DOI:10.3390/cells14020083
PMID:39851511
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11764157/
Abstract

Cannabinoid compounds have potential as treatments for a variety of conditions, with cannabigerol (CBG) being known for its anti-inflammatory properties. In this study, we investigated the effects of CBG in a cellular model of 1-chloro-2,4-dinitrobenzene (DNCB)-induced atopic dermatitis (AD). In the cellular model, we confirmed the cytotoxicity of CBG and downregulated the expression of inflammatory markers , , , and ( < 0.001). In the mouse model, clinical, histological, and immunological changes were analyzed. The results showed that CBG improved dermatitis severity score, epidermal thickness, and mast cell count and reduced inflammatory cytokines (, , , , , , , , and ) by qRT-PCR ( < 0.001). Western blot results showed modulated changes in JAK1, JAK2, TYK2, STAT1, STAT2, STAT3, p-STAT3, STAT6, and p-STAT6 ( < 0.05). Subsequently, p-IκBα, NF-κB, and p-NF-κB signaling factors were also reduced ( < 0.05), with corresponding changes in skin barrier factors. The results of this study indicate that CBG effectively alleviates AD-like symptoms and suggest the potential of CBG as a therapeutic agent.

摘要

大麻素化合物有潜力用于治疗多种病症,其中大麻二醇(CBG)以其抗炎特性而闻名。在本研究中,我们在1-氯-2,4-二硝基苯(DNCB)诱导的特应性皮炎(AD)细胞模型中研究了CBG的作用。在细胞模型中,我们证实了CBG的细胞毒性,并下调了炎症标志物 、 、 和 的表达(<0.001)。在小鼠模型中,分析了临床、组织学和免疫学变化。结果表明,通过qRT-PCR检测,CBG改善了皮炎严重程度评分、表皮厚度和肥大细胞计数,并降低了炎症细胞因子( 、 、 、 、 、 、 、 和 )(<0.001)。蛋白质免疫印迹结果显示JAK1、JAK2、TYK2、STAT1、STAT2、STAT3、p-STAT3、STAT6和p-STAT6有调节性变化(<0.05)。随后,p-IκBα、NF-κB和p-NF-κB信号因子也减少(<0.05),皮肤屏障因子有相应变化。本研究结果表明,CBG可有效缓解类AD症状,并提示CBG作为治疗剂的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b38/11764157/fbeae5033bb6/cells-14-00083-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b38/11764157/e41ea18aef96/cells-14-00083-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b38/11764157/9920076d7300/cells-14-00083-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b38/11764157/c8c2d8a42b17/cells-14-00083-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b38/11764157/0f697e927eed/cells-14-00083-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b38/11764157/ef81ccbbba19/cells-14-00083-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b38/11764157/fbeae5033bb6/cells-14-00083-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b38/11764157/e41ea18aef96/cells-14-00083-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b38/11764157/9920076d7300/cells-14-00083-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b38/11764157/c8c2d8a42b17/cells-14-00083-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b38/11764157/0f697e927eed/cells-14-00083-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b38/11764157/ef81ccbbba19/cells-14-00083-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b38/11764157/fbeae5033bb6/cells-14-00083-g006.jpg

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