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吲哚 - 3 - 甲醇通过抑制特应性皮炎中的骨膜蛋白/胸腺基质淋巴细胞生成素减轻过敏性皮肤炎症。

Indole-3-carbinol alleviates allergic skin inflammation via periostin/thymic stromal lymphopoietin suppression in atopic dermatitis.

作者信息

Kang Yun-Mi, Kim Hye-Min, Lee Junho, Baek Jong-Suep, Lee Minho, An Hyo-Jin

机构信息

Department of Herbology, College of Korean Medicine, Sangji University, Wonju, Gangwon-Do, 26339, Republic of Korea.

Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine (KIOM), 70 Cheomdan-Ro, Dong-Gu, Daegu, 41062, Republic of Korea.

出版信息

Chin Med. 2024 Dec 26;19(1):177. doi: 10.1186/s13020-024-01042-5.

Abstract

BACKGROUND

Atopic dermatitis (AD) is a chronic multifactorial inflammatory skin disorder with a complex etiology. Despite its increasing prevalence, treatment of AD is still limited. Indole-3-carbinol (I3C) is found in cruciferous vegetables and is formed when these vegetables are cut, chewed, or cooked; it exerts diverse pharmacological activities.

METHODS

HaCaT keratinocytes stimulated with tumor necrosis factor-α and interferon-γ mixture and NC/Nga mice stimulated with 2,4-dinitrochlorobenzen (DNCB) were used for AD models, in vitro and in vivo, respectively.

RESULTS

The results showed that I3C reduced the expression of pro-inflammatory cytokines, thymic stromal lymphopoietin (TSLP), and periostin in in vitro model. Oral administration of I3C alleviated AD-like skin inflammatory symptoms, including serum IgE levels, epidermal thickening, inflammatory cell infiltration, transepidermal water loss, and scratching behavior. Moreover, I3C decreased the expression of TSLP and periostin and recovered the expression of skin barrier proteins by regulating Aryl Hydrocarbon Receptor and inhibiting the mitogen-activated protein kinase and nuclear factor-κB pathways in the skin of DNCB-induced AD mice.

CONCLUSIONS

I3C is suggested as a potential therapeutic alternative for the treatment of AD by repressing allergic inflammatory pathways.

摘要

背景

特应性皮炎(AD)是一种病因复杂的慢性多因素炎症性皮肤病。尽管其患病率不断上升,但AD的治疗方法仍然有限。吲哚 - 3 - 甲醇(I3C)存在于十字花科蔬菜中,当这些蔬菜被切割、咀嚼或烹饪时会形成;它具有多种药理活性。

方法

分别在体外和体内,将用肿瘤坏死因子-α和干扰素-γ混合物刺激的HaCaT角质形成细胞以及用2,4 - 二硝基氯苯(DNCB)刺激的NC/Nga小鼠用于AD模型。

结果

结果表明,在体外模型中,I3C降低了促炎细胞因子、胸腺基质淋巴细胞生成素(TSLP)和骨膜蛋白的表达。口服I3C减轻了AD样皮肤炎症症状,包括血清IgE水平、表皮增厚、炎症细胞浸润、经表皮水分流失和搔抓行为。此外,I3C通过调节芳烃受体并抑制DNCB诱导的AD小鼠皮肤中的丝裂原活化蛋白激酶和核因子-κB途径,降低了TSLP和骨膜蛋白的表达,并恢复了皮肤屏障蛋白的表达。

结论

通过抑制过敏性炎症途径,I3C被认为是治疗AD的一种潜在治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/15ab/11670403/f87ded0d72aa/13020_2024_1042_Fig1_HTML.jpg

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