异甘草素通过JAK/STAT途径治疗小鼠特应性皮炎的机制研究

doi:10.3969/j.issn.1006-6233.2021.05.02

Abstract
Figure/Table
References
Related Citation (1)

Download: PDF (1509 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective: To investigate the mechanism of isoliquiritigenin in the treatment of atopic dermatitis in mice through Janus kinase-signal transducer and activator of transcription(JAK-STAT) pathway. Methods: Sixty SPF male C57BL/6 mice were randomly divided into negative control group, model group, isoliquiritigenin low dose group (50 mg/kg), isoliquiritigenin high dose group (100 mg/kg) and positive control group (prednisolone, 10 mg/kg), with 12 mice in each group. In addition to the negative control group, 2,4-dinitrochlorobenzene (DNCB) was smeared on the back depilated area and ears of mice in other groups to prepare atopic dermatitis (AD) model. On the first day after successful modeling, mice in isoliquiritigenin low dose group, isoliquiritigenin high dose group and positive control group were given corresponding drugs by gavage, while mice in negative control group and model group were given the same amount of distilled water once a day. After 14 consecutive days, the mice were evaluated for scratching behavior and dermatitis score, and serum interleukin-4(IL-4), tumor necrosis factor-α(TNF-α) and immunoglobulin E(IgE) levels, the levels of JAK1, JAK3, STAT3 and STAT6 protein in the skin tissue were detected. Results: The skin of mice in negative control group was normal; the skin of mice in the model group showed varying degrees of erythema, dryness, scratches, epidermal erosion and shedding, and scabs; the symptoms of the isoliquiritigenin low and high dose groups were significantly alleviated, and the isoliquiritigenin high dose group had obvious curative effect; the positive control group has better efficacy than that in the isoliquiritin high dose group. Compared with the negative control group, the number of scratches, dermatitis score, IL-4, TNF-α, IgE, JAK1, JAK3, STAT3 and STAT6 protein in the other groups were increased (P<0.05). Compared with the model group, the number of scratches, dermatitis score, IL-4, TNF-α, IgE, JAK1, JAK3, STAT3 and STAT6 protein in the isoliquiritin low dose group, isoliquiritin high dose group and the positive control group decreased, and the effect in the isoliquiritin dose groups was dose-dependent, but the effect was not as good as the positive control group (P<0.05). Conclusion: Isoliquiritin has therapeutic effect on the skin lesions of AD model mice, and its mechanism may be related to the inhibition of JAK-STAT pathway.

Key words： Isoliquiritigenin JAK-STAT pathway Atopic dermatitis

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	LI Yuanyuan
	PAN Xinfeng
	CHI Liqiao

Cite this article:

LI Yuanyuan,PAN Xinfeng,CHI Liqiao. Mechanism of Isoliquiritigenin in the Treatment of Atopic Dermatitis in Mice Through JAK-STAT Pathway[J]. HeBei Med, 2021, 27(5): 710-715.

URL:

http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2021.05.02 OR http://www.hbyxzzs.cn/EN/Y2021/V27/I5/710

[1] Vakharia PP,Silverberg JI.Adult-onset atopic dermatitis: characteristics and management[J].Am Clin Dermatol,2019,20(6):771~779.
[2] Katoh N,Ohya Y,Ikeda M,et al.Clinical practice guidelines for the management of atopic dermatitis 2018[J].Dermatol,2019,46(12):1053~1101.
[3] 魏海霞,孔伟,巩萍.异甘草素的药效学研究进展[J].药物生物技术,2019,26(5):467~470.
[4] Ye H,Yang X,Chen X,et al.Isoliquiritigenin protects against angiotensin Ⅱ-induced fibrogenesis by inhibiting NF-κB/PPARγ inflammatory pathway in human Tenon's capsule fibroblasts[J].Exp Eye Res,2020,199(1):108~146.
[5] Tang Y,Wang C,Wang Y,et al.Isoliquiritigenin attenuates LPS-induced AKI by suppression of inflammation involving NF-κB pathway[J].Am Transl Res,2018,10(12):4141~4151.
[6] Kahn J,Deverapalli SC,Rosmarin D.JAK-STAT signaling pathway inhibition: a role for treatment of various dermatologic diseases.[J].Semin Cutan Med Surg,2018,37(3):198~208.
[7] 陈振辉,李霞,韩立,等.芦荟提取物对特应性皮炎小鼠模型IgE、IL-17及NF-κB通路的影响[J].中国皮肤性病学杂志,2019,33(6):644~650.
[8] 郑梅,郝小龙,阴英,等.异甘草素减轻重症急性胰腺炎小鼠心肌损伤机制[J].中华老年心脑血管病杂志,2019,21(2):177~180.
[9] 蒙玉娇,李宁飞,翟春艳,等.清热除湿汤对NC/Nga小鼠特应性皮炎的作用研究[J].中华中医药杂志,2018,33(5):2056~2060.
[10] Lee HR,Kim TH,Oh SH,et al.Prednisolone-loaded coatable polyvinyl alcohol/alginate hydrogel for the treatment of atopic dermatitis[J].Biomater Sci Polym Ed,2018,29(13):1612~1624.
[11] 于辉,赵阳,费家玥,等.异甘草素抑制SETD7表达可保护缺氧/复氧诱导心肌细胞的氧化损伤[J].中国组织工程研究,2020,24(35):5613~5618.
[12] Vroman H,Bergen IM,van Hulst JAC,et al.TNF-alpha-induced protein 3 levels in lung dendritic cells instruct T(H)2 or T(H)17 cell differentiation in eosinophilic or neutrophilic asthma[J].Allergy Clin Immunol,2018,141( 5):1620~1633.
[13] Montilla AM,Gomez-García F,Gomez-Arias PJ,et al.Scoping review on the use of drugs targeting JAK/STAT pathway in atopic dermatitis,vitiligo,and alopecia areata[J].Dermatology Ther,2019,9(4):655~683.
[14] Dao TTP,Song K,Kim JY,et al.Igalan from Inula helenium (L.) suppresses the atopic dermatitis-like response in stimulated HaCaT keratinocytes via JAK/STAT3 signaling[J].Inflamm Res,2020,69(3):309~319.
[15] Miggelbrink AM,Logan BR,Buckley RH,et al.B cell differentiation and IL-21 response in IL2RG/JAK3 SCID patients after hematopoietic stem cell transplantation[J].Blood,2018,131(26): 2967~2977.