ETHNOPHARMACOLOGICAL RELEVANCE:The traditional Chinese herbal medicine called Xiao-bi decoction (XBD) has been used for decades to treat psoriasis, but its mechanism of action is poorly understood. AIM OF THE STUDY:To investigate the underlying mechanism of XBD against psoriasis using systematic pharmacological techniques. MATERIALS AND METHODS:A psoriasis model was established in mice using imiquimod (IMQ). The efficacy of XBD was evaluated based on psoriasis severity scores and immune cell infiltration. Core components and targets were screened using UPLC-QE-MS/MS and network pharmacology. The mechanism was further explored via transcriptome sequencing, ELISA, western blotting, immunolocalization, and molecular docking. RESULTS:XBD treatment significantly alleviated IMQ-induced psoriatic symptoms like erythema, scaling, and thickening. It reduced CD4+ T cell infiltration in skin and decreased serum levels of IL-17, IL-1β, IL-23, and IL-36. XBD specifically decreased CD4+-IL-17+ cells while increasing CD4+-FoxP3+ cells in both blood and skin. A total of 1223 chemical components were identified in XBD, including 78 blood-entering components. Network pharmacology and transcriptome analysis collectively demonstrate that XBD inhibits the activation of the JAK2/STAT3 signaling pathway, indicating its potential role in modulating this pathway. Our results also showed that XBD modulated Th17/Treg balance in serum and ameliorating skin inflammation in IMQ-induced psoriatic model. CONCLUSION:The herbal medicine Xiao-bi decoction may regulate the JAK2/STAT3 pathway, thereby influencing the Th17 response and Treg differentiation, and thereby alleviating the skin inflammation of psoriasis.

Pyoderma gangrenosum (PG) is a rare, chronic, autoinflammatory neutrophilic dermatosis. Its typical clinical manifestations include painful papules and pustules surrounded by erythema on the lower extremities and trunk, which gradually progress to form well-demarcated, painful ulcers with undermined edges. Due to impaired skin barrier function, prolonged wound exposure, and the frequent need for immunosuppressive therapy, PG patients are highly susceptible to secondary infections. We report here a clinical case of successful treatment with glucocorticoids and voriconazole, combined with multiple sessions of negative-pressure wound therapy and skin grafting, in a patient with cutaneous Aspergillus flavus infection and possible pyoderma gangrenosum.

Purslane is a traditional Chinese medicine with a long‑standing history of efficacy in the management of dermatological conditions such as vitiligo. However, the molecular mechanisms underlying its therapeutic effects on vitiligo remain unclear. Therefore, the present study explored these mechanisms using network pharmacology, molecular docking and in vitro experiments. Following the screening process, seven principal active components were identified, namely kaempferol, hesperetin, luteolin, quercetin, arachidonic acid, cycloartenol and β‑sitosterol. In addition, six key targets, namely AKT1, tumor protein p53, peroxisome proliferator‑activated receptor γ (PPARG), estrogen receptor 1, prostaglandin‑endoperoxidase synthase 2 and mitogen‑activated protein kinase 1, and eight pathways in purslane‑based vitiligo treatment were identified. Network pharmacology and molecular docking demonstrated that flavonoids are the key components of purslane likely to mitigate oxidative stress damage in vitiligo. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses revealed that the phosphatidylinositol 3‑kinase (PI3K)/AKT, p53 and PPARG signaling pathways are associated with purslane components and vitiligo. In vitro experiments revealed that purslane total flavones (PTF) increased cell viability, decreased ROS levels and increased antioxidant enzyme activities in H2O2‑induced B16F10 cells. In addition, PTF activated the PI3K/AKT signaling pathway in H2O2‑induced B16F10 cells, and the antioxidant effect of PTF was attenuated by a PI3K/AKT inhibitor. In conclusion, the findings of the present study suggest that the flavonoids of purslane contribute, at least in part, to its therapeutic effectiveness in vitiligo by mitigating oxidative stress in melanocytes through the PI3K/AKT signaling pathway.

Psoriasis is a chronic autoimmune disease marked by excessive keratinocyte growth and immune issues. Xiao Bi decoction (XBT), a traditional Chinese formula, has shown effective for treating psoriasis. This study integrated network pharmacology and Mendelian randomization analysis to explore the therapeutic mechanism of XBT and validate causal relationships between its active components, potential targets, and psoriasis outcomes. The results showed that XBT contains 171 active components, of which the top 5 active components with the highest degree values were quercetin, dihydrobaicalin _qt, Pyrethrin II, Kinobeon A, and Baicalein; the main core targets of XBT were tumor necrosis factor, interleukin (IL)-6, glyceraldehyde-3-phosphate dehydrogenase, AKT1, and IL-1B. These core components and core targets can be better molecular docking, and Mendelian randomization analysis showed that there is a causal relationship between the reduced level of IL-6 and the increased risk of psoriasis. These results provide novel insights into the molecular mechanisms and scientific validation of XBT's use in psoriasis.

Atopic dermatitis (AD) and psoriasis (Pso) are both recurrent inflammatory diseases. Recently, it has been reported that a small number of AD patients experience immune drift after receiving dupilumab treatment, leading to a transition from eczema-like lesions to psoriasis-like lesions. Here, we report a case of pustular psoriasis caused by dupilumab treatment for atopic dermatitis. This case underscores the diagnostic challenges associated with immune drift related to biological agents while also highlighting the shortened time frame for immune drift onset compared to previous reports.

Acne stands as a prevalent chronic inflammatory dermatological condition, typically characterized by concurrent skin inflammation and scarring. Currently, although many studies have been conducted on the pathogenesis of acne, a comprehensive understanding of its potential biomarkers is still pending. Key genes and immune cell characteristics associated with acne were investigated through bioinformatics analysis of transcriptomic data from acne patients in the public database GEO. A total of 198 significantly differentially expressed genes were identified in GSE6475 and GSE53795 datasets. Gene modules significantly associated with disease traits were identified by WGCNA network analysis, and their functional enrichment was further analyzed. The best diagnostic genes were LRRC17, TCN1, S100A12 and CCL19. The accuracy of the diagnostic model was verified by ROC curves and expression was validated in both datasets. GSEA functional enrichment analysis revealed the biological functions of these diagnostic genes. In addition, the analysis of immune cell scores by CIBERSORT algorithm revealed the differences in immune cells between acne patients and healthy patients, and found the correlation between multiple immune cells and diagnostic gene presentation. This bioinformatics study provides insights into the molecular mechanisms and immune regulation of acne and uncovers potential biomarkers that provide important clues for future disease diagnosis and treatment. Not applicable.

BACKGROUND:Psoriasis is a chronic autoimmune skin disease with unclear pathogenesis. It was found that miR-149-5p was significantly decreased in psoriatic lesion tissues. In this study, we aims to investigate the role and related molecular mechanism of miR-149-5p on psoriasis.METHOD:IL-22 was used to stimulate HaCaT and NHEK cells to establish psoriasis model in vitro. The miR-149-5p and phosphodiesterase 4D (PDE4D) expression levels were detected by quantitative real-time PCR. HaCaT and NHEK cells proliferation was determined by Cell Couting Kit-8 assay. The cell apoptosis and cell cycle were detected by flow cytometry. The cleaved Caspase-3, Bax and Bcl-2 protein expressions were detected by western blot. The targeting relationship between PDE4D and miR-149-5p was predicted and confirmed by Starbase V2.0 and dual-luciferase reporter assay, respectively.RESULT:There was a low expression level of miR-149-5p and a high expression of PDE4D in psoriatic lesion tissues. MiR-149-5p could target PDE4D. IL-22 promoted HaCaT and NHEK cells proliferation, while inhibited cell apoptosis and accelerated cell cycle. Moreover, IL-22 decreased the expressions of cleaved Caspase-3 and Bax, and increased the expression of Bcl-2. And the overexpressed miR-149-5p promoted HaCaT and NHEK cells apoptosis, inhibited cell proliferation and retarded cell cycle, meanwhile increased the cleaved Caspase-3 and Bax expressions, decreased the Bcl-2 expression. In addition, PDE4D overexpression has the opposite effect as miR-149-5p.CONCLUSION:The overexpressed miR-149-5p inhibits IL-22-stimulated HaCaT and NHEK keratinocytes proliferation, promotes cell apoptosis and retards cell cycle by down-regulating the expression of PDE4D, which could be the promising therapeutic target of psoriasis.

目的:通过基因表达数据库(GEO)芯片分析及分子对接方法探讨槲皮素对银屑病外周血中性粒细胞弹性蛋白酶(neutrophil elastase,NE)的分子机制.方法:从公共GEO下载GSE106087芯片数据,筛选差异靶点基因;收集中药系统药理学数据库与分析平台(traditional Chinese medicine systems pharma-cology database and analysis platform,TCMSP)中槲皮素预测靶点基因,与银屑病外周血NE差异性基因取交集,收集槲皮素干预银屑病外周血NE的靶标基因,并进行String平台验证,同时进行基因本体论功能富集分析(gene ontology,GO)和KEGG富集分析(kyoto encyclopedia of genes and genomes,KEGG),最后通过分子对接证据支持分析槲皮素干预银屑病NE的作用机制.结果:1)GSE106087基因芯片共包含基因49454个,银屑病外周血NE差异性基因189个(上调36个、下调153个);GO富集分析为432条生物过程、23条细胞成分、6条分子功能;KEGG富集分析为12条信号通路;2)槲皮素干预银屑病外周血NE差异基因11个(下调7个、上调4个),拓扑网络筛选核心靶标基因为JUN、SSP1(均为银屑病外周血NE上调基因),通过String平台验证为8个,其中能与槲皮素进行分子对接基因共6个,GO富集分析生物过程共291条、细胞成分7个、分子功能14个;KEGG富集分析为34条信号通路.结论:1)GSE106087基因芯片包含基因49454个,银屑病外周血NE的病理机制主要与ARG1等基因、中性粒细胞活化、病毒蛋白与细胞因子、细胞因子受体相互作用等上调,以及SPP1等基因、中性粒细胞脱颗粒生物过程、NOD样受体信号通路等下调关系密切;2)槲皮素干预银屑病外周血NE机制,主要与上调JUN、SSP1和下调IL-17信号通路、TNF信号通路等密切相关.

目的:观察PRP(富血小板血浆)联合凉血五花汤治疗激素依赖性皮炎的近期治疗效果及远期疗效.方法:选取激素依赖性皮炎患者,依据不同的治疗方案将研究对象分为观察组(28例)和对照组(30例),对照组予凉血五花汤加减口服,在保湿基础上外用牛碱性成纤维细胞生长因子;观察组在对照组治疗的基础上给予PRP治疗,比较两组的临床评分、VISIA分值及不良反应,12周后对患者进行微信随访,记录复发率.结果:两组患者治疗前后临床症状积分比较,均具有统计学差异(P＜0.05);两组治疗后VISIA红斑区域均具有统计学差异(P＜0.05);观察组纹理具有统计学差异(P＜0.05),而对照组纹理分值无统计学差异(P＞0.05).观察组及对照组的临床总有效率分别为96.43％、80.00％,差异有统计学意义(P＜0.05),观察组优于对照组.12周后随访,两组患者中,对照组有1例复发,两组均无明显不良反应发生.结论:PRP联合凉血五花汤比单独凉血五花汤药物治疗疗效更好.说明PRP是一种具有较高安全性,且整体疗效较好的治疗方法,值得临床推广.

Cutaneous squamous cell carcinoma (CSCC) is a common cancer in humans and is the second major type of skin cancer that causes death in humans. In this article, we investigated the effects of alkannin on CSCC progression. We revealed that alkannin curbed CSCC cell viability in a dose-dependent manner and accelerated CSCC cell apoptosis. In addition, alkannin expedited macrophage M1 polarization while curbing M2 polarization. Moreover, alkannin elevated phosphatase and tensin homolog (PTEN) abundance in CSCC cells. The results of bioinformatics analysis revealed that alkannin might modulate CSCC via PTEN. Downregulation of PTEN reversed the effects of alkannin on apoptosis of CSCC cells and M1/M2 polarization of macrophages. Alkannin reduced CSCC tumor growth in a mouse xenograft model. In conclusion, alkannin curbed the advancement of CSCC by expediting apoptosis and facilitating M1 polarization of macrophages by upregulating PTEN. These data may offer a therapeutic approach against CSCC.

1 病历摘要 患者男,30岁.因左足拇趾趾甲根部赘生物2年余于2019年12月16日至我科就诊.患者2年余前无明显诱因左足拇趾趾甲根部出现一丘疹样皮色赘生物,无疼痛瘙痒等不适,自行用指甲刀将其刮除,其后又反复生长,后患者未予处理,皮损逐渐增大至黄豆大,有压痛,并压迫甲板出现一纵向凹槽.患者既往体健,否认局部外伤史,家族成员中无类似疾病患者.

The interleukin-23 (IL-23)/IL-17 immune axis has been linked to the pathology of psoriasis, but how this axis contributes to skin inflammation in this disease remains unclear. We measured inflammatory cytokines associated with the IL-23/IL-17 immune axis in the serum of patients with psoriasis using enzyme-linked immunosorbent assays. Psoriasis was induced in male C57BL/6J mice using imiquimod (IMQ) cream, and animals received intraperitoneal injections of recombinant mouse anti-IL-23A or anti-IL-17A antibodies for 7 days. The potential effects of the IL-23/IL-17 immune axis on skin inflammation were assessed based on pathology scoring, hematoxylin-eosin staining of skin samples, and quantitation of inflammatory cytokines. Western blotting was used to evaluate levels of the following factors in skin: ACT1, TRAF6, TAK1, NF-?B, and pNF-?B. The serum of psoriasis patients showed elevated levels of several cytokines involved in the IL-23/IL-17 immune axis: IL-2, IL-4, IL-8, IL-12, IL-17, IL-22, IL-23, and interferon-?. Levels of IL-23p19 and IL-17 were increased in serum and skin of IMQ-treated mice, while ACT1, TRAF6, TAK1, NF-?B, and pNF-?B were upregulated in the skin. A large proportion of NF-?B p65 localized in nucleus of involucrin(+) cells in the epidermis and in F4/80(+) cells of the dermis of psoriatic lesional skin. Treating these animals with anti-IL-23 or anti-IL-17 antibodies improved pathological score and immune imbalance, mitigated skin inflammation and downregulated ACT1, TRAF6, TAK1, NF-?B, and pNF-?B in skin. Our results suggest that skin inflammation mediated by the IL-23/IL-17 immune axis in psoriasis involves activation of the ACT1/TRAF6/TAK1/NF-?B pathway in keratinocytes and macrophage.

该文报告 1 例难愈性皮肤溃疡病例,并讨论"煨脓长肉"中药换药法及富血小板血浆(PRP)治疗慢性难愈性皮肤溃疡的作用机制.该案患儿因"跑步机绞伤致皮肤严重破溃 1 个月余"就诊,接受几次伤口清创和简单的敷料包扎后未见效,通过多次"煨脓长肉"中药换药法(创面基础处理+碧玉散粉外用)联合PRP治疗后,皮损在 1 个月内完全愈合.

瘢痕疙瘩(keloid)是皮肤在创伤修复过程中由于成纤维细胞过度增殖、胶原过度沉积所形成的产物,其发病机制多而复杂,存在治疗抵抗和复发率高等类肿瘤特性,治疗方法繁多但单一治疗效果欠佳,是一种临床难治性疾病.除手术治疗外,药物注射(如曲安奈德、氟尿嘧啶、肉毒素、干扰素等)、光电治疗、冷冻治疗、压力治疗、放疗及洋葱提取物等均被应用于瘢痕疙瘩的治疗.

患者女,35岁.小腿白斑进行性增多6年,伴手臂白斑1年.前臂及小腿见多个散在分布的直径约0.5-1.5 cm圆形或类圆形白色斑片,界限清楚,表面光滑无鳞屑,周围皮肤颜色正常,白斑密集不融合,对称分布,触之皮温正常,摩擦白斑处后可见白斑颜色变淡甚至消失,高举手臂白斑颜色变淡.皮肤镜:摩擦皮损前,镜下见淡白色斑片及散在苍白色点,白斑内见不规则网状色素沉着及散在点球状血管;摩擦皮损后,镜下见淡白色斑片及散在苍白色点,白斑内见不规则网状色素沉着及点球状、线状分支状毛细血管.诊断:Marshall-White综合征.

带状疱疹是一种临床常见病,多由疱疹病毒感染引起,常侵害神经末梢,其表现为受侵害部位皮肤刺痛、烧灼痛、瘙痒等不适,严重影响人们的日常生活.近年来,有研究认为带状疱疹后遗神经痛可能是一种基于神经系统病理改变的神经性疼痛.西医治疗带状疱疹常用抗病毒、营养神经、对症止痛等方法,但疗效欠佳;中医治疗带状疱疹神经痛有其独特的优势,通过探讨桃红四物汤治疗带状疱疹后遗神经痛的理论机制,为临床治疗带状疱疹后遗神经痛提供一定的理论依据.

目的:基于网络药理学原理探讨消疕汤核心药对金银花-连翘干预银屑病的分子通路及作用机制.方法:应用中药系统药理学数据库与分析平台(traditional Chinese medicine systems pharmaco-logy database and analysis platform,TCMSP)检索金银花、连翘化学成分、作用靶点,并通过GeneCards数据库获取银屑病差异性靶点基因,预测中药与银屑病相关的作用靶点,通过STRING平台构建蛋白质-蛋白质相互作用信息网络(PPI),运用DAVID数据库对筛选出的靶点基因进行基因富集分析,获得基因本体论功能富集分析(gene ontology,GO)和KEGG富集分析(kyoto encyclopedia of genes and genomes,KEGG)信号通路注释结果,构建"中药成分-关键靶标-主要通路"的可视化网络图,探究金银花-连翘药对干预银屑病的分子作用机制.结果:金银花-连翘药对干预银屑病,共预测得到28个活性成分,涉及核心靶标基因127个,生物功能138个和信号通路155个.结论:金银花-连翘药对主要活性成分通过多靶点、多通路干预银屑病,主要涉及核受体的活性、转录因子活性、细胞因子受体结合、细胞因子生物功能等和白细胞介素17(interleukin-17,IL-17)信号通路、肿瘤坏死因子(tumor necrosis factor,TNF)信号通路、磷脂酰肌醇3-激酶(phosphati-dylinositol 3-kinase,PI3K)-蛋白激酶B(protein kinase B,Akt)信号通路等.

Platelet rich plasma (PRP) is a platelet concentrate obtained after autologous whole blood centrifugation.It is rich in a variety of growth factors, which can promote cell proliferation, matrix remodeling and angiogenesis, thus playing an antiinflammatory repair and tissue regeneration role.In recent years, it has been widely used in orthopedics, regenerative medicine,skin and so on.This article reviews the application and limitations of PRP in facial rejuvenation, scar repair, stria gravidarum and chloasma.

本文报道一例被误诊为泛发型湿疹的14岁的天疱疮患者。患者因全身散发绿豆至花生大小水疱、红斑、丘疹，伴瘙痒，反复搔抓后出现破溃，伴少许渗出，被外院诊断为“泛发型湿疹”，外用药物治疗效果不佳后前来我院就诊。患者全身皮肤干燥，头面部、颈部、胸腹、腰背、双上肢、双臀部、双小腿、双大腿见散在红斑，其上见花生至蚕豆大小水疱、丘疹，皮损以上半身为主，部分水疱疱液紧张，疱液清或少部分稍浑浊，水疱破溃后见潮红色糜烂面，伴淡黄色渗液，部分表面破溃后见黄褐色痂壳，散见暗褐色色素沉着，尼氏征阳性，以上皮损基本呈对称性分布。诊断：红斑型天疱疮。

患者男,43岁,6+年2型糖尿病史,反复口腔溃疡7+年,项部因毛囊炎形成溃疡面;入院前于院外输液治疗"腹痛",输液处表现针刺试验阳性,皮损处出现红斑、水泡,当时未予重视.入院后针刺处无明显反应,针刺试验阴性;入院后第二天转至皮肤科,在暗红色瘢痕增生面皮损基础上,出现不规则水泡的新皮损,针刺试验阴性,予相关治疗好转后出院.6月后随访,最初皮损严重处形成瘢痕疙瘩,形成陈旧性瘢痕增生面.