Background Dysregulated sphingolipid metabolism plays a key role in atopic dermatitis (AD), yet therapeutic options targeting this pathway remain limited. The traditional formula Peitu Qingxin (PTQX) shows clinical efficacy, but its molecular mechanism is largely undefined. Purpose To identify a novel mechanism of the PTQX formula in AD sphingolipid metabolism and to validate the miR-30a/GAPR-1 axis as a therapeutic target. Methods Using Mendelian randomization, clinical proteomics, and dual-luciferase reporter assays, we identified miR-30a as a direct upstream regulator of GAPR-1. Gain-of-function studies in AD-like 3D skin equivalents validated this axis. The effective dose of PTQX was determined in NC/Nga mice induced with 2,4-dinitrochlorobenzene. Molecular docking predicted the binding of PTQX components to GAPR-1. Adenovirus-mediated GAPR-1 silencing was performed in AD mice, and targeted lipidomics was used for detection. Finally, PTQX efficacy was evaluated in miR-30a knockout mice by assessing dermatitis severity, inflammatory cytokines/proteins, proteomics, and untargeted metabolomics. Results We found that miR-30a directly targets GAPR-1 and may exert a protective role in AD. In AD-like 3D skin equivalents, miR-30a overexpression downregulated GAPR-1, restored barrier proteins, and suppressed IL-8. Medium-dose PTQX treatment upregulated miR-30a and downregulated GAPR-1, concomitantly with amelioration of dermatitis. PTQX components were predicted to have strong binding affinity to GAPR-1 in silico. Adenovirus-mediated GAPR-1 silencing alleviated AD-like symptoms and restored sphingolipid metabolites. In miR-30a knockout mice, GAPR-1 expression was elevated. PTQX treatment suppressed serum levels of KC, IL-5, IL-12p70, IL-10, G-CSF, and TNF-α, reduced skin protein levels of NLRP3 and TLR2, and restored CYP1A1 expression. Multi-omics analyses further revealed that sphingolipid dysregulation is a key downstream mechanism. PTQX reversed the downregulation of key sphingolipid enzymes GBA and ENPP7, as well as 7 sphingolipid metabolites. Conclusion Targeting the miR-30a/GAPR-1 axis by PTQX represents a novel therapeutic approach for treating sphingolipid dysregulation in AD.

Atopic dermatitis (AD) is a chronic skin disease characterized by skin barrier dysfunction and immune balance disorders. Currently, drugs for repairing the skin barrier in AD are limited. The gu-ben-hua-shi formula (AESS) has been clinically validated in regulating Th1/Th2/Th17/Treg imbalance and barrier impairment in patients with AD; however, its underlying functional mechanism in repairing the skin barrier remain unknown. To elucidate the therapeutic effects of AESS on AD and to investigate its mechanism of restoring skin barrier function through the Hippo-YAP pathway. The main components of AESS were identified using UPLC-MS/MS. An observational study was conducted to evaluate the clinical efficacy of the AESS in patients with AD. Network pharmacology was used to predict the potential targets and mechanisms. AD mouse models were established by house dust mite stimulation in NC/Nga mice, and the effects on autophagy and the skin barrier were measured using western blotting, immunofluorescence, and transmission electron microscopy. The effects of AESS serum on AD-like inflammatory cell model were detected in HaCaT cells stimulated with interferon-γ (IFN-γ)/tumor necrosis factor-α (TNF-α). Activity of the Hippo-YAP signaling pathway was also investigated after YAP knockdown. Sixty major components were identified. AESS improved skin rash and barrier function, reduced eosinophil counts, and increased Th1/Th2 and Treg/Th17 ratios in patients with AD. AESS increased autophagy, improved skin barrier function, and inhibited Hippo-YAP signaling pathway activity. YAP knockdown reduces these therapeutic effects. Besides regulating immune imbalance, AESS increases keratinocyte autophagy levels, thereby restoring skin barrier function in AD through the Hippo-YAP signaling pathway.

Background and Purpose: Many people with atopic dermatitis seek treatment with Chinese herbal medicine (CHM). However, the evidence that informed clinical guideline recommendations is outdated. This research updates the evidence on the efficacy and safety of CHM for atopic dermatitis and supports clinical decision-making. Methods: Randomised controlled trials (RCTs) were identified from the World Health Organization’s International Clinical Trials Registry Platform. RCTs that compared CHM with a placebo, waitlist control or conventional medicine were eligible if they reported patient-reported outcomes, clinician-reported symptoms, long-term control, health-related quality of life or safety. Characteristics and results were extracted, risk of bias assessed and the certainty of evidence determined using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) framework. Meta-analysis was conducted where possible. Results: Seven RCTs (862 participants) were included. Topical CHM was not statistically different to placebo in reducing visual analogue scale itch score (MD −2.15 [−5.64, 1.34], I 2  = 95%; evidence not graded) but was more effective than placebo in reducing Eczema Area and Severity Index scores (MD −2.75 [−4.07, −1.44], I 2  = 0%; low certainty evidence). CHM was not statistically different to placebo in improving health-related quality of life (MD −2.20 [−5.27, 0.88], I 2  = 0%; moderate certainty evidence). More adverse events were reported in the CHM groups than in the comparator groups. Conclusion: There is limited evidence to support a change in clinical practice using CHM for atopic dermatitis. Future research should focus on patient-reported symptoms and clinician-reported signs and should carefully assess adverse events.

Atopic dermatitis (AD) is a chronic, recurrent inflammatory disease. Animal models are important for studying disease mechanisms and identifying new therapeutic agents. However, owing to AD heterogeneity and complexity, there is currently no mouse model that can fully simulate human AD. We searched experimental articles published between 2017 and 2021 to identify the most suitable AD mouse model. We summarized and compared 614 articles, including details on mouse strains, sex, age, irritants, modeling cycles, and spontaneous mouse models. BALB/c mice (45.3 %) were the most commonly used. Generally, 4–8-week-old mice were used, and 44 irritants were identified. The most common irritant was 2,4-dinitrochlorobenzene (DNCB), followed by Dermatophagoides farinae mite antigen extract (DfE). The modeling period was generally 21–30 days. There is no perfect AD animal model, and we suggest selecting the most suitable AD model based on previous research or using two or more models to meet experimental requirements. When exploring allergies and T cell differentiation, it is recommended to use DNCB and DfE separately or in combination to stimulate BALB/c mice and NC/Nga mice for constructing AD models. If researchers want to explore the differentiation of Th17 and Th2 cells, the use of flaky tail mice is recommended. If researchers want to conduct research from the perspective of transcriptomics, it is recommended to increase the construction of IL-23 injected mice.

Traditional Chinese medicine (TCM) is a well-accepted therapy for atopic dermatitis (AD). However, there are currently no evidence-based guidelines integrating TCM and Western medicine for the treatment of AD, limiting the clinical application of such combined approaches. Therefore, the China Association of Chinese Medicine initiated the development of the current guideline, focusing on key issues related to the use of TCM in the treatment of AD. This guideline was developed in accordance with the principles of the guideline formulation manual published by the World Health Organization. A comprehensive review of the literature on the combined use of TCM and Western medicine to treat AD was conducted. The findings were extensively discussed by experts in dermatology and pharmacy with expertise in both TCM and Western medicine. This guideline comprises 23 recommendations across seven major areas, including TCM syndrome differentiation and classification of AD, principles and application scenarios of TCM combined with Western medicine for treating AD, outcome indicators for evaluating clinical efficacy of AD treatment, integration of TCM pattern classification and Western medicine across disease stages, daily management of AD, the use of internal TCM therapies and proprietary Chinese medicines, and TCM external treatments. Please cite this article as: Du XR, Wu MY, Tao MC, Lin Y, Gu CY, Wu MF, Cao Y, Chen DC, Li W, Wang HW, Wang Y, Wang Y, Lu HZ, Liu X, Su XF, Li FL. Clinical practice guidelines for the diagnosis and treatment of atopic dermatitis with integrative traditional Chinese and Western medicine. J Integr Med. 2025; 23(6):641-653.

IntroductionPrevious studies have demonstrated that gut microbiota and its metabolites, short-chain fatty acids (SCFAs), are involved in the inflammatory manifestations and immune regulation of atopic dermatitis (AD). However, their potential associations and mechanisms remain unclear.MethodsThis study used antibiotics to construct a mouse model to analyze the performance of AD mice after gut microbiota destruction. 16S rRNA amplicon sequencing combined with HM700 high-throughput metabolomics was used to characterize differential microbial components and key metabolites in fecal specimens of AD murine models. Moreover, the mechanism of action of the key metabolite was investigated.ResultsAfter antibiotic treatment, AD murine models demonstrated exacerbated clinical manifestations, characterized by enhanced dermatitis severity, significant ear edema, and elevated inflammatory responses. 16S rRNA sequencing revealed significant changes in the Bacteroidetes/Firmicutes ratio, while HM700 identified acetate as an important regulatory metabolite in AD mice. Acetate supplementation in AD mice significantly ameliorated 2,4-dinitrobenzene (DNCB)-induced dermatitis, as evidenced by reduced skin lesion severity, lower dermatitis scores, and decreased epidermal thickening. Mechanistically, acetate attenuated allergic responses by binding to free fatty acid receptor 2 (FFAR2) and suppressing the Th2 pathway through GATA binding factor 3 downregulation, along with marked reductions in serum immunoglobulin E and thymic stromal lymphopoietin levels. Notably, acetate administration did not alter gut microbiota composition or relative abundances.ConclusionOur results revealed that the ratio of Bacteroidetes/Firmicutes and low levels of acetate play important regulatory roles in AD, and exogenous supplementation of acetate can alleviate DNCB-induced AD in mice through the FFAR2 and Th2 pathways. These findings provide valuable insights into the mechanisms of AD occurrence and progression, microbial community dynamics, metabolic regulation, and functional food innovation.

IntroductionAtopic dermatitis (AD) is characterized by skin barrier dysfunction and inflammation.This study explored the relationship between Yes-associated protein (YAP) expression, autophagy, and skin barrier dysfunction in AD.MethodsSkin samples from AD patients and healthy controls were analyzed using mRNA-seq. Differential gene expression was visualized using ggplot2 and analyzed using GO and KEGG pathway analyses. An AD mouse model was created using house dust mite ointment, and HaCaT cells were treated to mimic AD inflammation. YAP expression was transfected with lentivirus in vivo and siRNA in vitro. Autophagy was induced with rapamycin.ResultsYAP levels were reduced in AD patients and correlated with filaggrin (FLG). YAP overexpression in mice improved skin lesions, enhanced barrier function (increased FLG, involucrin, and loricrin), and promoted autophagy (increased LC3-II/I; decreased p62 and p-mTOR). Similar effects were observed in cells, with increased proliferation and reduced apoptosis. YAP knockdown reversed these effects, which were mitigated by rapamycin.DiscussionReduced YAP expression in AD is linked to inflammation and barrier dysfunction. YAP may improve AD by enhancing autophagy, reducing inflammation, and restoring skin barrier function.

Traditional Chinese medicine（TCM） clinical thinking can be categorized as holistic thinking,dialectical thinking,balanced thinking,common thinking and pattern thinking. Balanced thinking is the core of the five types of thinking,and can be used in the interpretation of health and disease,the construction of a model of human equilibrium, the diagnosis of disease, the determination of therapeutic principles, and the implementation of specific treatment methods. The syndrome differentiation, and classification of syndrome patterns and theoretical models of TCM are all aimed to restore the holistic balance by following the holistic concept of “man being an integral part of nature”. Balanced thinking is implemented through the whole process of exploring the commonalities of the syndromes,performing syndrome differentiation and treatment,and achieving holistic harmony,which is the core thinking of TCM clinical practice.

Clinical curative effect is the core value and fundamental pursuit of medicine. The data-driven clinical quantitative evaluation model is an important research issue in clinical efficacy evaluation. The existing clinical efficacy evaluation methods have made a lot of contributions to the structured information of static attributes, but less attention is paid to the heterogeneous information with dynamic and random characteristics. This paper discusses a class of clinical efficacy evaluation decision-making problems that contain both time-series and dynamic characteristics and uses the three-way decision principle to describe these characteristics. The group decision-making theory is introduced to aggregate the evaluation information of time series dynamic features generated in the decision-making process. A time series dynamic three-way group decision model for clinical efficacy evaluation is constructed, the optimal decision rules with minimum expected loss objective are calculated and proofed in the proposed model, and then the optimal treatment alternative is obtained. Finally, taking the decision-making problem of clinical efficacy evaluation of traditional Chinese medicine (TCM) treatment of atopic dermatitis as the research object, based on the actual clinical data of Guangdong Provincial Hospital of TCM, the decision-making process and steps of the theoretical model constructed in this paper are verified and applied. The data-driven quantitative clinical evaluation model has achieved better application effects than the actual clinical scenarios. The research results in this paper provide new ideas and theoretical methods for real-world clinical efficacy evaluation research.

Gu-ben-hua-shi (AESS) formula is a clinical experienced prescription from Guangdong Hospital of Traditional Chinese Medicine (TCM), which is used to treat atopic dermatitis (AD). Our previous work has shown that AESS has therapeutic effect on AD by regulating yes-associated protein (YAP). AESS formula has multi-component and multi-target characteristic, and need to be analyzed by systematic chemical profiling and network pharmacology technology, as well as verification of key signaling pathways. Therefore, this study aimed at investigating the efficacy and effect of AESS formula in the treatment of AD and its effect on NLRP3 signaling pathway. The components of AESS formula were analyzed and identified by ultra high performance liquid chromatography/tandem mass spectrometry (UHPLC- MS/MS), and the potential mechanism of AESS formula in the treatment of AD was predicted by network pharmacology approach, with detected main components, and the potential components targeted NOD-like receptor thermal protein domain associated protein (NLRP3) signaling pathway [Direct binding with NLRP3, apoptosis-associated speck-like protein (ASC) and Caspase-1] were assessed using molecular docking. AD-like symptoms were constructed by DNCB induced BALB/c mice. The effect of AESS formula on dorsal skin structure in AD-like mice was observed using H E staining. Furthermore, the western blotting experiment explored the expression of the NLRP3 pathway protein. By UHPLC-MS/MS analysis, 91 compounds were detected in AESS formula, and 76 of them were identified, while by network pharmacological analysis, 1500 component targets were obtained, and 257 of them were obtained by intersection with eczema targets. Then one of the key pathways, nucleotide-binding oligomerization domain (NOD)-like signaling pathway was obtained by KEGG enrichment analysis. Molecular docking results showed 24 main components could effectively combine with ASC and Caspase-1 (≤−7 kcal/mol). The animal experiment results further showed that AESS formula alleviates symptoms in AD-like mice. ELISA kit results showed that the expression of IL-1β and IL-18 in serum was inhibited after AESS treatment. Additionally, western blotting analysis showed that the expressions of ASC, Caspase-1 and NLRP3 protein expression in the skin tissue of mice were down-regulated after AESS treatment. The experimental results show that AESS formula inhibited the expression of NLRP3 signaling pathway for the treatment of AD. AESS formula can improve AD symptoms in mice by inhibiting the activation of NLRP3 inflammasome and the expression of the related downstream inflammatory cytokines.

BACKGROUND:This systematic review evaluated the Chinese herbal medicine (CHM) for treating atopic dermatitis (AD). METHODS:PubMed, EMBASE, the Cochrane library, the Wanfang database, and China National Knowledge Infrastructure (CNKI) were searched for relevant randomized controlled trials (RCTs) from inception to December 2021. Overall recovery rate, disease/symptom severity scoring, quality of life (QoL), recurrence rate, and incidence of adverse events (AEs) were evaluated. STATA SE 14.0 software was used for statistical analysis. RESULTS:17 RCTs involving 1624 patients were eligible. CHM was associated with a higher overall recovery rate (risk ratio [RR] = 1.15, 95% confidence interval [CI]: 1.05, 1.26, p = .003) and decreased recurrence rate (odds ratio [OR] = 0.19, 95% CI: 0.07, 0.55, p = .002), both confirmed by sensitivity analyses. CHM could decrease scoring atopic dermatitis index (MD = -0.61, 95% CI: -1.12, -0.11, p = .017), however, sensitivity analysis revealed non-robustness. No significant differences were found between the CHM and the control group in Eczema Area and Severity Index, QoL, and the incidence of AEs. CONCLUSIONS:CHM was effective for treating AD as it could improve the overall recovery rate and decrease the recurrence rate. More studies are required to validate the potential of CHM on disease/symptoms severity and QoL.

特应性皮炎是一种慢性炎症性皮肤病,其病理机制涉及表皮屏障功能破坏、皮肤微生物组异常和2型炎症免疫失调之间复杂的相互作用.随着组织工程技术发展,3D皮肤模型已与正常人体皮肤结构接近.通过模拟特应性皮炎的病理机制,许多研究者成功构建出特应性皮炎的3D皮肤模型.该模型被应用于特应性皮炎的病理机制研究、药物筛选方面,是进行特应性皮炎研究的重要工具.故本文对现有的特应性皮炎3D皮肤模型构建方法及其在AD研究中的应用进行综述,并阐述其存在问题及未来发展方向,为学者应用3D皮肤模型研究特应性皮炎提供参考.

湿,属六气之一.湿证是指具有湿之特性的各种不同证候.近年来,湿证是中医证候研究的热点和重点具有重要的科学研究价值,证候的构建是中医与现代医学的桥梁和纽带.构建能客观体现及反映湿证的动物模型是进一步开展临床和基础研究的立足点.目前,已有很多的中医湿证实验室研究报道,尤其在各种中医湿证动物模型的构建及相关指标的检测.现对中医湿证的理论源流、湿证动物模型分类及湿证模型检测指标及意义的研究进展进行探讨,为中医湿证动物模型的建立及优化研究提供参考及启示,以期为湿证动物模型的构建及湿证生物学机制研究提供思路.

Background: Atopic dermatitis (AD) is a complex inflammatory skin condition characterized by the proliferation and activation of immune cells in skin. Isoliquiritin (ISO) is an active component purified from Glycyrrhiza glabra. This study aimed to test the therapeutic potential of ISO for AD and verify its potential molecular mechanism. Methods: This study investigated the potential effects and possible underlying mechanisms of ISO against AD in vitro (HMC1.1 cells stimulated by phorbol-12-myristate-13-acetate and calcium ionophore A23187) and in vivo (AD-like mouse model induced by 1-chloro-2,4-dinitrochlorobenzene). Results: ISO dose-dependently suppressed the viability of HMC1.1 cells. ISO inhibited the secretion of the proinflammatory factors IL-6 and IL-8 and induced the apoptosis of HMC1.1 cells. ISO suppressed the phosphorylation of CD177, JAK2, STAT1, STAT3, and STAT5, and upregulated the protein expression of BAX and cleaved caspase-3 in vitro. ISO administration markedly diminished the infiltration of immune cells (mast cells, eosinophils) in cutaneous lesions. Simultaneously, ISO treatment alleviated the formation of skin lesions and affected other AD symptoms (thickness of the epidermis and dermis, ear edema, lymph node weight, spleen index, dermatitis score) but increased the thymus index in vivo, and downregulated expression of IL-4, IL-6, IgE, and thymic stromal lymphopoietin (TSLP). Conclusions: Collectively, our findings showed that ISO administration decreased skin lesion formation by inhibiting inflammation and enhancing immunomodulation through the CD177/JAK2/STAT signaling pathway.

神经性皮炎属于中医学"牛皮癣""摄领疮"范畴,是一种以阵发性剧痒和皮肤苔藓样变为特征的慢性炎症性皮肤病,其病程长、易复发、难治愈.陈达灿教授基于多年临证经验认为本病在早期发作时与肝密切相关,治疗重在从肝论治,以清肝火、祛肝风、疏肝经、调肝血为主,慢性肥厚期多证属脾湿血瘀,治当健脾除湿、活血除瘀通络,施以"三术三藤"验方加减.具体选择药物方面,不仅善于针对病机精选药味,注重一药多用,充分发挥药物功效,还贵在随次症灵活加减,从而使全方达到药少力专之效.本文从病因病机、治疗思路和用药特色逐层解析其临证经验,并附验案以详细说明和佐证.

Background: Atopic dermatitis (AD) is a chronic and recurrent skin disease. At present, there is a lack of sufficiently effective and safe medicines that can be used for a prolonged time and reduce the recurrence of AD. The Gu-Ben-Hua-Shi (AESS) formula has been used for many years with a good clinical effect on AD but its specific treatment mechanism is unknown. Methods: The main components of AESS were analyzed using ultra-high performance liquid chromatography (UPLC). The composition of AESS compounds in the serum from rats was analyzed using ultra-high performance liquid chromatography-mass spectrometry. An AD mouse model was constructed using 2,4-dinitrofluorobenzene stimulation in Balb/C mice and the effect on the reduction of skin lesions and Th1/Th2/Th17/Treg balance after AESS administration were measured. The effects of AESS serum on the proliferation and apoptosis of keratinocyte cell line HaCaT and adhesion of HaCaT to human monocyte cell line THP-1 were detected in an IFN-γ/TNF-α stimulated AD-like inflammatory cell model. The effects of Yes-associated protein (YAP) expression on the therapeutic effect and a related signaling pathway were also investigated. Results: In total, 10 components were confirmed using UPLC, namely five organic acids, three flavonoids, and two chromogenic ketones. Additionally, the similarity of the three batches of samples (S1–3) was above 0.98, indicating that the formula samples have good uniformity. These 10 compounds were also detected in rat serum, suggesting that they are absorbed into rat blood as prototype components. Furthermore, AESS effectively reduced the skin lesions in the AD mouse model, regulated the Th1/Th2/Th17/Treg imbalance, improved the proliferation ability of the AD-like cell model, and inhibited HaCaT apoptosis and adhesion to THP-1 cells. It also reduced the expression of YAP in Th17 and Treg cells of the mouse spleen and increased YAP expression in the skin. The change in YAP expression in keratinocytes weakened the curative effect of AESS, and AESS exerted its effects through the NF-κB signaling pathway. Conclusion: AESS may play a role in the treatment of AD by affecting the expression of YAP. These findings can be used to promote its use as an alternative medication for prolonged use with fewer side effects.

总结陈达灿教授治疗脂溢性皮炎的临证经验.在病因病机方面,陈达灿教授认为,阴虚和脾虚是本病发病和反复发作的根本原因,风湿热邪则为本病标实.临证治疗时,重在辨证补虚,以滋补肾阴、健运脾胃、疏风清热利湿为主要治则,标本兼治;治疗过程中始终重视顾护脾胃;用药上,善用动物类药和引经药,并对青蒿有独到的见解和使用,从而增强全方疗效.诊治特色明显,临床疗效显著.

目的 观察培土清心方对人肥大细胞HMC1.1突变株与HMC1.2突变株细胞增殖活性及对HMC1.1突变株相关信号通路的影响,为中医药复方治疗特应性皮炎提供实验依据.方法 (1)培土清心方实验组不同剂量(0.01 mg/mL、0.05 mg/mL、0.1 mg/mL、0.25 mg/mL、0.5 mg/mL、1.0 mg/mL)分别作用于HMC1.1及HMC1.2细胞,采用Cell Counting Kit-8检测培土清心方对HMC1.1及HMC1.2细胞增殖活性的影响.(2)采用Western blot方法检测培土清心方实验组不同剂量(0.25 mg/mL、0.5 mg/mL、1.0 mg/mL)对HMC1.1细胞C-kit/Stat信号通路的作用.结果(1)培土清心方0.25 mg/mL、0.5 mg/mL、1.0 mg/mL分别作用48小时均能显著抑制HMC1.1与HMC1.2细胞增殖活性(P<0.05),并且呈现一定的剂量依赖性.培土清心方0.25 mg/mL、0.5 mg/mL、1.0 mg/mL分别作用HMC1.1与HMC1.2细胞72小时也呈现剂量依赖性抑制细胞增殖活性作用.尤其是对HMC1.1细胞增殖抑制更为明显.(2)培土清心方对HMC1.1细胞作用8小时后,使Phospho-C-kit(Y703)蛋白表达具有下调趋势,以及一定量降低Phospho-C-kit(Y719)蛋白表达的作用.培土清心方对HMC1.1细胞作用8小时后,使Phospho-Stat1(Y701)/Stat1蛋白表达具有下调趋势,并且呈现出剂量依赖性.结论 实验结果表明培土清心方对人肥大细胞HMC1.1增殖抑制的作用机制可能涉及C-kit/Stat信号通路,对肥大细胞的作用可能是培土清心方治疗特应性皮炎的潜在作用机制之一.

系统总结了陈达灿教授治疗寻常型银屑病的学术思想和经验.通过临床跟诊学习及病案整理,从病因病机、辨证分型及用药对陈教授经验进行归纳和总结,最后辅以验案加以佐证.陈教授认为岭南地区银屑病的发病以热(血热、或兼风热)、瘀(血瘀)为主,常兼湿邪为患.临床分为血热证、血瘀证、脾虚湿蕴证,治以清热凉血、活血祛瘀、健脾祛湿化瘀,并且根据多年临床经验,形成自己独特的用药特点,常配伍解毒药物使用,在临床取得显著的疗效.

Psoriasis and skin tumors (such as basal cell carcinoma, squamous cell carcinoma, and melanoma) are chronic diseases that endanger physical and mental health, and yet the causes are largely unknown and treatment options limited. The development of targeted drugs requires a better understanding of the exact pathogenesis of these diseases, and Yes-associated protein (YAP), a member of the Hippo signaling pathway, is believed to play an important role. Psoriasis and skin tumors are characterized by excessive cell proliferation, abnormal differentiation, vasodilation, and proliferation. Here, we review the literature related to YAP-associated disease mechanisms and discuss the latest research. YAP regulates cell apoptosis, proliferation, and differentiation; inhibits cell density and intercellular contacts and angiogenesis; and maintains the three-dimensional structure of the skin. These mechanisms may be associated with the occurrence and development of psoriasis and skin tumors. The results of recent studies have shown that YAP expression is increased in psoriasis and skin tumors. High expression of YAP in psoriasis and skin tumors may indicate its positive functions in skin inflammation and malignancies and may play an important role in disease pathogenesis. The study of new drugs targeting YAP can provide novel approaches for the treatment of skin diseases.