BACKGROUND:There is an unmet treatment need and a lack of efficacy evidence for Huoxiang Zhengqi (HXZQ) oral liquid for atopic dermatitis (AD). OBJECTIVES:To assess the therapeutic efficacy and safety profile of HXZQ therapy in adult Chinese patients with AD or eczema. METHODS:In the CHARM study (a multi-center, double-blind, randomized controlled trial), randomized participants with mild AD or eczema received HXZQ or a placebo for 4 weeks randomly. The primary outcome was the change in the Eczema Area and Severity Index (EASI) scores from baseline to the end of treatment. Several secondary outcomes were also measured. RESULTS:In total, 218 participants were enrolled who received either HXZQ (n = 110) or a placebo (n = 108). The adjusted difference in the change in the EASI score from baseline to Week 4 between the two groups was -0.44 (95 % confidence interval [CI]:0.83, -0.04; p = 0.033) in the intention-to-treat analysis. At Week 8, 70 participants (66 %) in the HXZQ group had a 50 % or greater reduction from baseline in the EASI score, as compared with 53 participants (50.5 %) in the placebo group (p = 0.022). LIMITATIONS:Only mild AD or eczema participants were observed; due to the limited 4-week treatment timeframe, HXZQ oral liquid's long-term clinical benefits could not be fully determined. CONCLUSIONS:In participants with mild AD/eczema, treatment with HXZQ oral liquid resulted in greater EASI reduction than treatment with placebo at Week 4, and had more benefits in skin clearance benefits over 8 weeks.

Ethnopharmacological relevance: Psoriasis is characterized by hyperkeratosis that produces the classic silvery scales, and the pathogenesis of psoriasis involves abnormal proliferation of keratinocytes. Emerging evidence supports that apoptosis regulates keratinocyte proliferation and formation of stratum corneum, which maintains the homeostasis of the skin. Qinzhuliangxue mixture (QZLX) is a representative formula for the treatment of psoriasis, which was earliest recorded in the classic Chinese medicine book Xia's Surgery. In our previous clinical studies, QZLX demonstrated 83.33% efficacy with few side effects in the treatment of psoriasis. Furthermore, our published basic research has also proved that the QZLX mixture effectively inhibits the hyperproliferation of keratinocytes, thus exerting therapeutic effects on psoriasis. However, whether QZLX mixture can regulate keratinocytes apoptosis requires further clarification. Objective of the study: To investigate the mechanism of QZLX in the treatment of psoriasis from the perspective of keratinocyte apoptosis. Materials and methods: First, psoriasis-like mice with imiquimod (IMQ)-induced were given QZLX intragastric administration and Psoriasis Area Severity Index (PASI) scores were recored for 11 consecutive days to appraise the efficacy. Then, tissue samples were collected for transcriptome analysis. The DEseq2 method detected significantly differentially expressed genes (DEGs), Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) Pathway databases were used to analyze the functions and pathway enrichment of DEGs. After that, the therapeutic mechanisms of QZLX in intervening with psoriasis were explored using TUNEL, immunohistochemical staining, and western blotting. Results: QZLX ameliorated the symptoms and pathological characteristics of IMQ-induced psoriasis in mice. The epidermal cell hyperplasia in the skin was inhibited, in accordance with the suppressed expression of PCNA and Ki67 after treatment. Transcriptome sequencing showed that melanoma differentiation associated gene-5 (MDA5) was downregulated. GO and KEGG enrichment analysis of the signaling pathways indicated that the differentially expressed genes were significantly enriched in apoptosis pathways. Besides, QZLX treatment decreased the apoptosis of keratinocyte as shown by reduced TUNEL-positive cells. As MDA-5 protein levels decreased, so did the expression of the downstream protein Caspase-8, which indicates that the apoptotic pathway was triggered. Furthermore, QZLX therapy might also help to balance the apoptotic Bcl-2 family expression. Conclusion: QZLX restrains the apoptosis of keratinocyte in psoriasis-like mice by downregulating the MDA-5 pathway. The restoration of the balance between cell apoptosis and proliferation in the skin may lead to considerable psoriasis relief. Our study reveals the possible molecular processes behind the effects of QZLX therapy on the skin lesions of psoriasis, and lends support to its clinical efficacy.

Background: Psoriasis is a long-lasting, inflammatory, continuous illness caused through T cells and characterized mainly by abnormal growth and division of keratinocytes. Currently, corticosteroids are the preferred option. However, prolonged use of traditional topical medication can lead to adverse reactions and relapse, presenting a significant therapeutic obstacle. Improved alternative treatment options are urgently required. Formononetin (FMN) is a representative component of isoflavones in Huangqi (HQ) [Astragalus membranaceus (Fisch.) Bge.]. It possesses properties that reduce inflammation, combat oxidation, inhibit tumor growth, and mimic estrogen. Although FMN has been shown to ameliorate skin barrier devastation via regulating keratinocyte apoptosis and proliferation, there are no reports of its effectiveness in treating psoriasis. Objective: Through transcriptomics clues and experimental investigation, we aimed to elucidate the fundamental mechanisms underlying FMN's action on psoriasis. Materials and methods: Cell viability was examined using CCK8 assay in this study. The results of analysis of differentially expressed genes (DEGs) between FMN-treated HaCaT cells and normal HaCaT cells using RNAsequencing (RNA-seq) were presented on volcano plots and heatmap. Enrichment analysis was conducted on DEGs using Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO), and results were validated through RT-qPCR verification. After 12 days of FMN treatment in psoriasis mouse model, we gauged the PASI score and epidermis thickness. A variety of techniques were used to assess FMN's effectiveness on inhibiting inflammation and proliferation related to psoriasis, including RT-qPCR, HE staining, western blot, and immunohistochemistry (IHC). Results: The findings indicated that FMN could suppress the growth of HaCaT cells using CCK8 assay (with IC50 = 40.64 uM) and 20 uM FMN could reduce the level of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) to the greatest extent. FMN-treated HaCaT cells exhibited 985 up-regulated and 855 down-regulated DEGs compared to normal HaCaT cells. GO analysis revealed that DEGs were linked to interferon (IFN) signaling pathway. Furthermore, FMN improved pathological features, which encompassed decreased erythema, scale, and thickness scores of skin lesions in psoriasis mouse model. In vivo experiments confirmed that FMN downregulated expression of IFN-alpha, IFN-beta, IFN-gamma, decreased secretion of TNF-alpha and IL-17 inflammatory factors, inhibited expression of IFN-related chemokines included Cxcl9, Cxcl10, Cxcl11 and Cxcr3 and reduced expression of transcription factors p-STAT1, p-STAT3 and IFN regulatory factor 1 (IRF1) in the imiquimod (IMQ) group. Conclusions: In summary, these results suggested that FMN played an anti-inflammatory and anti -proliferative role in alleviating psoriasis by inhibiting IFN signaling pathway, and FMN could be used as a potential therapeutic agent.

Ethnopharmacological relevance: Psoriasis is a chronic inflammation and relapsing disease that affected approximately 100 million individuals worldwide. In previous clinical study, it was observed that the topical application of Si Cao Formula (SCF) ameliorated psoriasis skin lesions and reduced the recurrence rate of patients over a period of three months. However, the precise mechanism remains unclear. Aim of the study: The objective of this study was to assess the effectiveness and safety of SCF in patients diagnosed with psoriasis and explore the molecular mechanisms that contribute to SCF's therapeutic efficacy in psoriasis treatment. Materials and methods: A randomized, controlled, and pilot clinical study was performed. This study assessed 30 individuals diagnosed with mild to moderate plaque psoriasis. 15 of them underwent local SCF treatment, the others received calcipotriol intervention. The outcome measure focused on Psoriasis Area and Severity Index (PASI), Dermatology Life Quality Index (DLQI), and recurrence rate. In addition, IMQ-induced psoriasis-like mice model were used to assess the impact of SCF on ameliorating epidermal hyperplasia, suppressing angiogenesis, and modulating immune response. Furthermore, we performed bioinformatics analysis on transcriptome data obtained from skin lesions of mice model. This analysis allowed us to identify the targets and signaling pathways associated with the action of SCF. Subsequently, we conducted experimental validation to confirm the core targets. Results: Our clinical pilot study demonstrated that SCF could ameliorate skin lesions in psoriasis patients with comparable efficacy of calcipotriol in drop of PASI and DLQI scores. SCF exhibited a significantly reduced recurrence rate within 12 weeks (33.3%). Liquid Chromatography Mass Spectrometry (LC-MS) identified 41 active constituents of SCF (26 cations and 15 anions). Animal experiments showed SCF ameliorates the skin lesions of IMQ-induced psoriasis like mice model and suppresses epidermal hyperkeratosis and angiogenesis. There were 845 up-regulated and 764 down-regulated DEGs between IMQ and IMQ + SCF groups. GO analysis revealed that DEGs were linked to keratinization, keratinocyte differentiation, organic acid transport epidermal cell differentiation, and carboxylic acid transport interferon-gamma production. KEGG pathway analysis showed that SCF may play a vital part through IL-17 and JAK/STAT signaling pathway. In addition, SCF could reduce the number of positive cells expressing PCNA, CD31, pSTAT3, CD3, and F4/80 within the epidermis of psoriatic lesions, as well as the expression of Il-17a and Stat3 in IMQ-induced psoriasis mice. Conclusions: Our research suggests that SCF serves as a reliable and efficient local approach for preventing and treating psoriasis. The discovery of plausible molecular mechanisms and therapeutic targets associated with SCF may support its broad implementation in clinical settings.

目的:探讨季德胜蛇药片治疗急性期带状疱疹的临床疗效.方法:将 176例急性期带状疱疹患者随机分为对照组与治疗组,各 88 例.对照组给予伐昔洛韦片口服及 0.9%生理盐水局部外敷治疗,治疗组给予伐昔洛韦片口服及季德胜蛇药片局部外敷治疗,疗程 7 d.治疗后 28 d评估患者临床疗效,治疗前、治疗后 7、14、28 d比较两组视觉模拟量表(VAS)、皮肤病生活质量指数(DLQI)评分,并记录不良反应发生情况.结果:治疗组总有效率高于对照组;止疱、结痂、脱痂时间等均短于对照组;治疗第 7、14、28 天,治疗组VAS和DLQI评分均低于对照组(P＜0.05);两组治疗过程中头晕、胃部不适、腹泻发生率比较差异无统计学意义.结论:季德胜蛇药片治疗急性期带状疱疹疗效好,可减轻疼痛,促进皮疹消退及创面愈合.

BACKGROUND AND AIMS:Psoriasis is a relatively common autoimmune inflammatory skin disease with a chronic etiology. Since psoriasis is still incurable, it is necessary to identify the molecular mechanisms of psoriasis. The present study was designed to detect novel biomarkers and pathways associated with psoriasis incidence, and provide new insights into treatment of psoriasis.METHODS AND RESULTS:Differentially expressed genes (DEGs) associated with psoriasis in the Gene Expression Omnibus (GEO) database were identified, and their functional roles and interactions were then annotated and evaluated through GO, KEGG, and gene set variation (GSVA) analyses. In total 197 psoriasis-related DEGs were identified and found to primarily be associated with the NOD-like receptor, IL-17, and cytokine-cytokine receptor interaction signalling pathways. GSVA revealed significant differences between normal and lesional groups (P < 0.05), while PPI network analyses identified CXCL10 as the hub gene with the highest degree value, whereas IRF7, IFIT3, OAS1, GBP1, and ISG15 were promising candidate genes for the therapeutic treatment of psoriasis.CONCLUSION:The findings of the present integrated bioinformatics may enhance our understanding of the molecular events occurring in psoriasis, and these candidate genes and pathways together may prove to be therapeutic targets for psoriasis.

目的 观察龙葵银消片联合阿维A胶囊治疗中重度寻常型银屑病血热证的临床效果及安全性.方法 将134例中重度寻常型银屑病血热证患者随机分为治疗组(67例)和对照组(67例).治疗组予龙葵银消片联合阿维A胶囊口服,对照组予阿维A胶囊口服,两组均外用尿囊素维他乳膏,治疗12周.比较两组患者临床疗效、银屑病面积及严重程度指数(PASI)评分、视觉模拟评分(VAS)、皮肤病生活质量指数(DLQI)、汉密尔顿抑郁量表(HAMD)和不良反应发生情况.结果 最终共纳入130例患者,治疗组66例,对照组64例.治疗组有效率(87.50％)高于对照组(70.00％)(P＜0.05).两组治疗后PASI、VAS、DLQI、HAMD评分均较治疗前显著降低(P＜0.05).治疗组在改善PASI和瘙痒上优于对照组(P＜0.05);而两组间DLQI、HAMD评分差异无统计学意义(P＞0.05).治疗组口干发生率为4.55％,明显低于对照组的18.75％(P＜0.05);两组患者治疗过程中眼干、高脂血症、甲沟炎发生率比较差异无统计学意义(P＞0.05).结论 龙葵银消片联合阿维A胶囊较单用阿维A胶囊治疗中重度寻常型银屑病血热证的临床疗效更佳,同时可减少阿维A胶囊导致的不良反应,更好地改善瘙痒症状,值得临床推广应用.

目的 探讨人参皂苷化合物K(CK)对H2O2诱导来自新生儿中度色素沉着性包皮的正常人表皮黑素细胞(HEMn-MP)细胞凋亡的保护作用及可能机制.方法 采用磷酸激酶抗体阵列检测HEMn-MP细胞各阵列蛋白磷酸化水平;比色法测定各组HEMn-MP细胞半胱天冬酶(Caspase-3)活性.结果 CK减弱H2O2诱导的HEMn-MP细胞P53蛋白磷酸化;CK降低H2O2诱导的Caspase-3活化.结论 人参皂苷CK可能通过抑制细胞凋亡对H2O2诱导的黑素细胞损伤有保护作用,因而可作为治疗白癜风的潜在药物.

目的 观察长波紫外线1(UVA1)光疗联合润肤膏走罐治疗斑块型银屑病的临床疗效.方法 选取105例斑块型银屑病患者,随机分为3组,剔除脱落病例后,治疗组(32例)、对照组A(31例)和对照组B(32例).治疗组给予UVA1光疗联合润肤膏走罐疗法治疗;对照组A给予走罐疗法治疗;对照组B给予UVA1光疗治疗.观察3组患者治疗前后皮损面积和严重程度评分(PASI)、皮肤病生活质量评分(DLQI)及临床疗效.同时,采用酶联免疫吸附测定(ELISA)法检测治疗前后血清白细胞介素-17(IL-17)、IL-23、肿瘤坏死因子-α(TNF-α)的表达水平变化.结果 治疗组总有效率为(93.75％),明显优于对照组A(80.64％)和对照组B(84.38％,P<0.05).3组治疗后PASI和DLQI评分,血清IL-17、IL-23、TNF-α的表达水平与同组治疗前比较显著降低,差异有统计学意义(P<0.05);与对照组比较,治疗组的各项观察指标均显著低于对照组,差异有统计学意义(P<0.05).结论 UVA1光疗联合润肤膏走罐疗法能明显改善斑块型银屑病患者皮损情况、提高生活质量,其作用机制可能与抑制血清IL-17、IL-23、TNF-α的表达水平,从而阻断IL-23/辅助性T细胞17(Th17)炎性轴相关.

Objective:This study aimed to investigate key biomarkers and their molecular pathogenesis in psoriasis. Methods:Differentially expressed genes (DEGs) of datasets (GSE13355, GSE30999, and GSE106992) obtained from Gene Expression Omnibus (GEO) were identified using Venn diagram. Function and pathway enrichment analyses were performed. Protein-protein interaction (PPI) network and the hub genes were constructed. The correlation between normal tissue and infiltrating immune cells was analyzed by CIBERSORT. ROC analysis was performed to distinguish between skin lesion samples and skin non-lesion samples. Analyze the highest expression of single gene in the whole body within the Human Protein Atlas (HPA) database. Effect of CXCL8 expression level on proliferation, invasion, migration and apoptosis of HaCat cells was detected by qPCR. Results:A total of 239 pairs of normal and lesional skin samples were downloaded. PPI network revealed a tight interaction among 197 DEGs. The GO enrichment analysis showed that these genes were markedly enriched in the "defense response to virus", "type I interferon signaling pathway", and "cell response to type I interferon" categories. The KEGG pathway analysis showed that the DEGs were mainly in the NOD-like receptor axis, interaction between cytokine and cytokine receptor and the IL-17 axis. PPI analysis showed that CXCL8 was the novel hub gene of psoriasis and correlated to 22 types of infiltrating immune cells. 6 miRNAs were predicted to be related to CXCL8. CXCL8 was most widely distributed in lymphoid tissues and plays a role in psoriatic inflammatory lesions by promoting cell proliferation, migration, and anti-apoptosis. Conclusion:CXCL8 plays a key role in psoriasis development. This study provided new insights into the exploration of molecular mechanisms and therapeutic targets of psoriasis.

银屑病是一种由免疫介导的慢性炎症性皮肤病,病理以角质形成细胞过度增殖、角化不全为其重要特征.自噬,指的是一类细胞的自我降解过程,将多余或受损的细胞器与蛋白质清除.如果在缺少细胞代谢能量的情况下,细胞采用自噬的方式,可以循环利用细胞内的成分,保持良好的自我稳态,维持基本的生存状态.在最近几年以来,许多研究结果显示,在许多免疫炎症性皮肤病中,均会产生细胞自噬变化的病理过程.一些治疗银屑病的药物也可以采用细胞自噬的方式,起到良好的治疗效果.经研究后发现,应用中草药进行治疗,可以对细胞自噬产生良好的调控作用.笔者通过概括近十余年来银屑病中自噬的国内外研究现状,为银屑病的治疗提供一个全新的方向,自噬可能成为治疗银屑病的一个新的靶点,中药诱导细胞自噬的研究将为治疗银屑病中药新药的研发提供新的方向.

带状疱疹是由水痘-带状疱疹病毒（VZV）引起的一种皮肤病，常伴有剧烈疼痛，部分患者尤其老年人容易并发带状疱疹后遗神经痛（PHN），严重影响患者的生活质量。中西医结合在治疗带状疱疹及预防PHN方面取得了一定进展；重组带状疱疹疫苗的研发与上市更是为高风险人群预防带状疱疹提供了可能，具有广大的发展前景。本文就西医抗病毒、止痛和尚存争议的糖皮质激素使用问题，中医中药，及疫苗的应用情况做一综述，为临床防治提供参考。

Bullous pemphigoid (BP) is a kind of immune bullous disease that often occurs in the elderly. Skin lesions manifest as pruritus papules or urticaria-like rash, accompanied by tension bullae. Immunopathology showed linear deposition of C3 and IgG in epidermal basement membrane, and anti-IgG autoantibodies in serum. The mechanism of BP is the interaction between autoantibodies and BP antigens (BP180/collagen XVII and BP230) in the hemidesmosomes of basal keratinocytes.1 Current treatments include topical and systemic use of glucocorticoids and other immunosuppressants. According to relevant reports, penicillin,2 captopril,3 teneliglipten,4 metamizole,5 erlotinib6 can all cause drug-induced BP (DIBP). However, no reports of apatinib mesylate inducing BP have been published. Herein, we present a case of DIBP triggered by oral apatinib mesylate and whose diagnosis was clinically and histopathologically confirmed. A 62-year-old Chinese woman presented with a 2-week history of flaky erythema and multiple blisters accompanying the oral mucosa to be affected was admitted to our hospital. In 2007, the patient was diagnosed with malignant breast tumour and underwent surgical treatment. From January 2019, she began to take megesterone acetate dispersible tablets (H20010074, 160 mg orally each day) and apatinib mesylate tablets (H20140103, 0.5 g orally each day) for the treatment of malignant breast tumour. Two weeks before presentation, the left neck and chest presented patchy erythema with itching. Ten days later, it had spread to the neck, trunk, upper limbs and bilateral groins, with severe itching and local blisters and bullae, erosion and pain of oral mucosa, accompanied by pharynx pain and cough (Figure S1a–b). An initial diagnosis of dermatitis medicamentosa was made, while discontinuation of apatinib mesylate and antiallergic medication was ineffective. Physical examination revealed scattered erosive surfaces in buccal mucosa and palate, massive oedematous erythema in neck, trunk, upper limbs and groins, some of which were targetoid in shape. Tensive blisters and bullae were locally visible, filled with yellowish fluid, and the Nikolsky sign was negative. A skin biopsy from the left forearm showed a subepidermal blister (Figure S2). Negative results were obtained in both direct and indirect immunofluorescence. Enzyme linked immunosorbent assay test showed that BP180 antibody was 84.3 U/mL (normal range, < 20 U/mL), desmin 1/3 antibody and BP230 antibody were all normal. Since the immunofluorescence test was negative, we performed another immunohistochemical test and the results were positive7 (Figure 1). The diagnosis of DIBP from apatinib mesylate was made based on the above clinical signs and examinations. The targeted drug was discontinued and the patient was cured after 14 days of methylprednisolone 60 mg/d intravenous drip treatment. Oral prednisone (25 mg daily) was started. All of the lesions resolved in 2 months and no relapse over the 5-month follow-up was observed. No recurrence was found after 2 months of follow-up. Apatinib mesylate tablets, an oral vascular endothelial growth factor receptor-2 (VEGFR-2) inhibitor, which has been approved as advanced gastric adenocarcinoma or gastric–oesophageal junction adenocarcinoma patients after the failure of second-line therapy. In addition, clinical studies have shown that apatinib has good antitumour activity against other solid tumours. Commonly reported side effects of apatinib include leukopenia, granulocytopenia, thrombocytopenia, proteinuria, hypertension, fatigue, hoarseness. Hand–foot syndrome (palms, plantar redness and pain or erythema at the tip of fingers) is the most common skin reaction after taking medicine. DIBP is not common, with the first case reported in 1970 in an 11-year-old boy receiving salicylazosulphapyridine.8 Currently, 50 drugs9 have been reported to induce BP, including antibiotics, antiarrythmics, antihypertensives, vaccines, nonsteroidal anti-inflammatory drugs, salicylates and diuretics. A systematic summary of DIBP is made and the following characteristics are found: younger age of onset, positive Nikolsky sign, appearance of lesions on normally appearing skin, involvement of lower leg areas, target lesions on palms and soles, mucosal involvement, marked eosinophilic infiltrate, intraepidermal vesicles, necrotic keratinocytes, thrombus formation, marked eosinophilia (serum), improvement after administration of systemic corticosteroids, improvement after discontinuation of specific drug, low rates of recurrence.10 To our knowledge, this is the first report of apatinib-induced BP. In the presented case, the patient was a middle-aged woman with severe damage of oral mucosa, and the rash extended to the lower limbs. The therapeutic effect of methylprednil was significant. We conducted antihistamine treatment according to drug eruption with poor efficacy. After skin biopsy, laboratory examination and immunohistochemical, BP was confirmed, and the rashes were significantly improved after 2 weeks of methylprednil treatment. However, we do not know for sure whether pemphigoid is associated with immune disorders caused by malignant tumours. In the future, the number of drugs thought to induce BP is likely to increase as new antineoplastic drugs develop. Three-year action plan (ZY(2018–2020)-ZYBZ-38). There are no competing interests to declare. Y.M. and F.S. diagnosed and treated the patient. Q.W. and X.S. analysed the results. W.J. searched the literature. Q.Z. and S.X. wrote the manuscript. FIGURE S1a Supporting Information FIGURE S1b Supporting Information FIGURE S2 Supporting Information Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

促进血管新生、改善微循环是创面修复的重要环节,因而治疗慢性难愈性创面应以促进微循环为主,在早期改善受损皮肤的血流状态和微循环,减少血栓形成以及炎性因子聚集,促进血管新生,提高蛋白表达水平.本研究就丹参、血竭、水蛭素、黄芪、黄蜀葵花以及其他具有改善微循环作用的中药及中药单体对于创面愈合的药理和临床研究做一综述,分析影响创面愈合的相关因素,对进一步探索安全高效的临床治疗药物有参考意义.

Background: Psoriasis is a relatively common autoimmune inflammatory skin disease with a chronic etiology. The present study was designed to detect novel biomarkers and pathways associated with psoriasis incidence. Methods: Differentially expressed genes (DEGs) associated with psoriasis in the Gene Expression Omnibus (GEO) database were identified, and their functional roles and interactions were then annotated and evaluated through GO, KEGG, and gene set variation (GSVA) analyses. In addition, the STRING database was leveraged to construct a protein-protein interaction (PPI) network, and key hub genes from this network were validated as being relevant through receiver operating characteristic (ROC) curve analyses of three additional GEO datasets. The CIBERSORT database was additionally used to assess the relationship between these gene expression-related findings and immune cell infiltration. Results: In total 197 psoriasis-related DEGs were identified and found to primarily be associated with the NOD-like receptor, IL-17, and cytokine-cytokine receptor interaction signaling pathways. GSVA revealed significant differences between normal and lesional groups (P < 0.05), while PPI network analyses identified CXCL10 as the hub gene with the highest degree value, whereas IRF7, IFIT3, OAS1, GBP1, and ISG15 were promising candidate genes for the therapeutic treatment of psoriasis. ROC analyses confirmed that these 6 hub genes exhibited good diagnostic efficacy (AUC > 70%), and were predicted to be associated with increased sensitivity to 10 drugs (P < 0.01). The CIBERSORT database further predicted that these hub genes were associated with infiltration by 22 different immune cell types. Conclusion: These results offer a robust foundation for future studies of the molecular basis for psoriasis, potentially guiding efforts to treat this common and disruptive disease.

目的 观察督灸配合走罐疗法治疗静止期寻常型银屑病的临床疗效.方法 将108例静止期寻常型银屑病患者随机分为治疗组和对照组,每组54例.治疗组采用督灸配合走罐治疗,对照组采用口服阿维A胶囊治疗.观察两组治疗前后银屑病面积及严重度指数(PASI)评分、皮肤病生活质量指数(DLQI)评分及血清白细胞介素(IL)-17、IL-22、IL-23水平的变化情况,并比较两组临床疗效及不良反应发生率.结果 两组治疗后PASI评分、DLQI评分及血清IL-17、IL-22、IL-23水平与同组治疗前比较,差异均具有统计学意义(P<0.01).治疗组治疗后PASI评分、DLQI评分及血清IL-17、IL-22、IL-23水平与对照组比较,差异均具有统计学意义(P<0.05).治疗组总有效率和不良反应发生率分别为83.3％和5.6％,对照组分别为72.2％和11.1％,两组总有效率比较,差异具有统计学意义(P<0.05).结论 督灸配合走罐能显著改善静止期寻常型银屑病患者皮损症状和生活质量,其机制可能与调节血清IL-17、IL-22、IL-23水平有关.

Background: Eczema is the most common allergic skin disorder in the world. The treatment of eczema with western medicine generally involves antihistamines, antibiotics, glucocorticoids, and immunomodulatory preparations, which are limited by common relapse events following drug withdrawal. Many traditional Chinese medicines have demonstrated significant effects on eczema; however, high-quality clinical studies are lacking. Objectives: We performed a multi-center, randomized, double-blind, clinical trial to evaluate the efficacy and safety of a Chinese herbal medicine, Qinzhuliangxue (QZLX) granules, and its effect on recurrence of eczema. Methods: A total of 342 patients with eczema who met the inclusion criteria were recruited and randomly divided into a traditional Chinese medicine (TCM) treatment group, a Western medicine (WM) treatment group, and a TCM plus WM treatment group, according to random numbers generated using the central stratified zone group random method. The Eczema Area and Severity Index (EASI) score and the level of pruritus were set as the primary outcome measures, and the Dermatology Quality of Life Index (DLQI) score served as the secondary outcome measure. In this study, a two-sided p-value less than 0.05 was considered statistically significant. Results: The median EASI score and the pruritus level at baseline were not statistically significant. However, as the treatment period progressed, the EASI score (including the total score and scores for the head, upper limb, trunk, and lower limb) and pruritus level decreased significantly in all three treatment groups. Repeated measures Analysis of Variance (ANOVA) demonstrated that the DLQI scores in the TCM, WM, and TCM+WM groups decreased significantly over time. Limitations: Basic experiments need to be increased. Conclusions: The Chinese herbal medicine QZLX granules significantly improved the EASI score and decreased the pruritus level in eczema patients, with good safety and no obvious adverse reactions. Trial Registration The protocol for this study was registered with the Clinical Trials database (NCT02517957). Registered 1 May 2015, Xia Shi Surgical Treatment for Eczema Multi-center Clinical Research - Full Text View - ClinicalTrials.gov

Background: Psoriasis is a chronic and prevalent skin condition brought on by various genetic and external factors. Till date, there is no cure for this disease. It is, therefore, crucial to examine the underlying mechanisms leading up to psoriasis. The goal of our study was to explore the mechanistic pathways involved in the molecular pathogenesis of psoriasis. Methods: Using Gene Expression Omnibus (GEO), we performed an extensive analysis of the transcript expression profile in psoriasis patients. The datasets GSE13355, GSE30999, and GSE106992, containing 239 pairs of normal and psoriatic skin samples were arbitrarily assigned to two non-overlapping cohorts for cross-validated differential gene expression analysis. The gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment and gene set enrichment analysis (GSEA) were employed for interpretation, visualization, and unified recognition. The STRING database was used to construct the protein–protein interaction (PPI) network and the hub genes were established using Cytoscape. Additionally, both differentially regulated genes and functional likeness of hub genes were further examined in terms of gene activation and functional outcome. The correlation between normal tissue and infiltrating immune cells was analyzed by CIBERSORT. Moreover, ROC analysis was performed to distinguish between skin lesion samples and skin non-lesion samples. In addition, a signaling axis involving lnRNA, miRNA, mRNA, and ceRNA was generated with information from the DEmiRNA, DElncRNA, and DEmiRNA-DEmRNA relationship. Lastly, immunohistochemical evaluations were used to analyze the highest expression of single gene in the whole body within the Human Protein Atlas (HPA) database. Results: The genetic profiles of 239 pairs of normal and lesional skin samples were downloaded from three datasets in the GEO database. PPI network revealed a tight interaction among 197 differentially expressed genes (DEGs). Moreover, gene ontology analyses indicated that psoriasis-related DEGs mostly included viral defense genes, type I interferon axis, and its corresponding cellular responses. The Kyoto encyclopedia of genes and the DEGs enrichment analysis showed involvement of the NOD-like receptor signaling network, cytokine-cytokine receptor binding, and IL-17 signaling axis in psoriasis verses non-psoriatic tissues. GSEA analysis demonstrated that CXCL8 was only enriched in the "complement characteristic" pathway. ROC curves indicated that CXCL8 expression was highly effective in classifying both lesional and non-lesional skin samples (with AUC 0.941, 0,935, and 0.794 for GSE13355, GSE30999, and GSE 106992). Furthermore, CIBERSORT database indicated that CXCL8 was correlated to 22 types of infiltrating immune cells. In addition, 6 miRNAs were predicted to be related to CXCL8, including hsa-miR-1294, hsa-miR-140-3p, hsa-miR-185-5p, hsa-miR-4306, hsa-miR-4644, and hsa-miR-493-5p. Lastly, immunohistochemical analysis showed that CXCL8 was most widely distributed in lymphoid tissues. Conclusions: Based on our analysis, CXCL8 plays a key role in psoriatic development. Our comprehensive bioinformatics analysis of the GEO data provided new insights into the exploration of molecular mechanisms while searching for highly efficient therapeutic targets for treating psoriasis.

Sanqi, a traditional Chinese herb, is widely used for cardiovascular diseases, and its neuroprotective effects against oxidative stress were recently discovered. The purpose of this study was to investigate whether Sanqi-derived compound K (Sanqi-CK), an active metabolite of Sanqi, could protect melanocytes from oxidative stress. Cultured human primary skin epidermal melanocytes (HEMn-MPs) were treated with hydrogen peroxide (H2O2) in the presence or absence of Sanqi-CK. Sanqi-CK exhibited protective effects against H2O2-induced cell death by reducing oxidative stress. In addition, treatment with Sanqi-CK reversed the decreased glutathione reductase activity and decreased ratio of reduced glutathione (GSH)/oxidized glutathione (GSSG) seen in H2O2-treated melanocytes. Furthermore, topical application of Sanqi-CK alleviated leukoderma in guinea pigs, a disorder characterized by melanocyte cell death resulting from rhododendrol-induced oxidative stress. Taken together, these data suggest that Sanqi-CK protects melanocytes against oxidative stress, and its protective effects are associated with modulating the redox balance between GSH and GSSG and activating glutathione reductase. Thus, Sanqi-CK may be a good candidate for preventing melanocyte loss in oxidative-stress-associated pigmentary disorders.

目的 探讨疱疹后神经痛(postherpetic neuralgia,PHN)患者采用电针针刺督脉穴、夹脊穴、背俞穴的治疗效果,比较三种穴位的疗效差异.方法 将入组的120例PHN患者随机分成A、B、C、D四组,每组30例.其中,A组口服普瑞巴林胶囊治疗;B、C、D三组在A组的基础上分别加用电针针刺督脉穴、夹脊穴、背俞穴治疗.观察和比较治疗前后四组患者的疼痛情况视觉模拟评分(visual analogue scale,VAS)、失眠情况匹兹堡睡眠质量指数(Pittsburgh sleep quality index,PSQI)评分.结果 A、B、C、D四组总有效率分别为80.0％、96.7％、96.7％、93.3％.B、C、D三组总有效率显著高于A组(P＜0.05),而B、C、D三组之间比较,差异无统计学意义(P＞0.05).A、B、C、D四组在T1至T4时间点的VAS、PSQI评分均显著低于同组T0时间点(P＜0.05),B、C、D三组较A组更优(P＜0.05);四组在T1、T2、T3、T4相同时间点的VAS、PSQI评分比较,B、C、D三组显著低于A组(P＜0.05);B、C、D三组间比较差异无统计学意义(P＞0.05).结论 电针针刺治疗督脉穴、夹脊穴、背俞穴联合普瑞巴林治疗在改善PHN患者疼痛、失眠方面效果显著,疗效均优于单独口服普瑞巴林;电针针刺在脊神经分布范围内均有效.