Atopic dermatitis (AD) is a chronic inflammatory skin disorder that significantly impacts patients’ quality of life. Although emerging research highlights the role of microbial dysbiosis in AD, the precise mechanisms of interaction between the skin and gut microbiota in the context of AD remain poorly understood. This systematic review synthesizes findings from studies comparing the microbiomes of AD patients and healthy controls, with a focus on the advances in amplicon sequencing and metagenomic sequencing. Seventeen studies, encompassing 665 AD patients and 768 healthy controls, were included in the review. These studies demonstrated significant microbial diversity shifts in AD patients, including a reduction in microbial diversity and shifts in specific microbial populations. These microbial alterations are thought to contribute to immune dysregulation, which plays a key role in AD pathogenesis. However, despite the growing body of evidence, the complex interactions between skin and gut microbiota and their exact contributions to AD remain insufficiently explored. This review highlights the need for further research into the gut-skin microbiome axis in AD, with an emphasis on how these microbial changes could lead to novel therapeutic strategies. Potential interventions such as probiotics, prebiotics, or other microbiome-based therapies could offer new treatment options for AD patients. The findings underscore the importance of continued investigation into microbial pathogenesis in AD to better inform future therapeutic approaches.

Psoriasis is a chronic, recurrent, immune-mediated inflammatory skin disease in which the TNF/IL-23/IL-17 axis plays a central role in the maintenance of mature plaques. However, this classical framework does not fully explain the early immune events triggered by skin injury, barrier disruption, infection, and the release of self-nucleic acids. It also does not fully explain selected clinical phenotypes. Type I interferons (IFN-I) are inducible cytokines involved in antiviral defense and danger sensing that may shift from protective immune mediators to pathogenic inflammatory amplifiers in psoriasis-prone skin. Self-nucleic acids released after tissue injury can form immunostimulatory complexes with antimicrobial peptides such as LL37. These complexes activate innate immune responses and induce IFN-I production. This process can promote dendritic-cell maturation and amplify the IL-23/IL-17 inflammatory pathway. This review presents IFN-I as a stage-dependent and phenotype-specific immune module that links early danger sensing to subsequent inflammatory amplification in psoriasis. We focus on the protective role of IFN-I in skin danger responses, LL37-mediated abnormal nucleic acid sensing, multicellular IFN-I skin signatures, the stage-specific integration of IFN-I with the IL-23/IL-17 axis, and clinical contexts with increased IFN-I activity. Moreover, we briefly discuss the therapeutic significance of tyrosine kinase 2 as a convergence node for IL-23, IL-12, and IFN-I signaling. Defining the role of IFN-I across different lesion stages and clinical phenotypes may improve the immunopathological model of psoriasis. It may also provide a basis for disease stratification, response prediction, and individualized therapy.

Psoriasis is a chronic immune-mediated inflammatory disease whose pathogenesis is a triad of genetic predisposition, immune dysregulation, and environmental triggers. This review provides a novel, in-depth synthesis arguing that microbial dysbiosis is not merely an associative phenomenon but a central regulatory node within this triad, actively shaping immune responses and clinical phenotypes. We move beyond cataloging microbial shifts to construct a detailed mechanistic framework of the gut-skin axis. Gut dysbiosis; characterized by reduced diversity, a diminished Bacteroidetes/Firmicutes ratio, and depleted SCFA producers, compromises intestinal barrier integrity, reduces systemic immunoregulatory tone via diminished SCFA signaling, and promotes Th17 polarization. This systemic inflammation is directly communicated to the skin. Concurrently, cutaneous dysbiosis, featuring Staphylococcus aureus dominance and fungal alterations, disrupts the local barrier, provides chronic antigenic stimulation, and amplifies IL-17-driven inflammation, creating a self-sustaining loop. Crucially, we analyze how specific infections (HCV, H. pylori, Streptococcus) act as environmental triggers by sharing or activating these very pathways. The bidirectional relationship with therapy is dissected: while biologics induce drug-specific microbiome shifts that often correlate with clinical normalization, they also carry infection risks that must be strategically managed. Emerging microbiome-targeted interventions like specific probiotics show promise but are hampered by methodological inconsistencies. This review uniquely highlights the causality gap and proposes that future breakthroughs require a shift from correlation to mechanism. We conclude that the microbiome is a dynamic interface between genes and environment in psoriasis; its successful integration into diagnostic and therapeutic paradigms demands standardized multi-omics approaches, functional validation, and personalized medicine strategies that target this critical axis.

BACKGROUND:Psoriasis treatment still requires further exploration. Fire needle therapy, an external method used in traditional Chinese medicine (TCM), is considered to have a definite effect on psoriasis, but lacks high-level clinical evidence. OBJECTIVE:To determine the efficacy and safety of fire needle therapy for psoriasis treatment. METHODS:This randomized, single-blind, multicenter clinical trial was conducted in five large hospitals in China. In total, 78 patients with plaque psoriasis aged 18 years or older were randomized to receive either fire needle therapy or control therapy over 4 weeks, with a 4-week follow-up. The full analysis and intention-to-treat sets were used for statistical analysis. RESULTS:After treatment, the Psoriasis Area and Severity Index (PASI) score in the fire needle therapy group was significantly lower (-1.15 ± 1.10 [95% confidence interval, CI: -1.51, -0.79] vs. -2.72 ± 2.15 [95% CI: -3.47, -1.97], P < 0.01), while the PASI50, PASI75 and PASI90 scores were substantially higher than those of the control group (77.14% vs. 42.11%, 57.14% vs. 21.05%, and 40.00% vs. 0%, P < 0.01). Fire needle therapy significantly improved the quality of life of patients with psoriasis (7.03 ± 4.01 [95% CI: 5.73, 8.33] vs. 3.66 ± 3.32 [95% CI: 2.50, 4.82], P < 0.05), with no adverse reactions. Further, there was no significant difference in recurrence rates between the two groups (0% vs. 6.06%, P > 0.05). CONCLUSION:Fire needle therapy is an effective and safe treatment for plaque psoriasis which improves patient quality of life. These findings support its use and suggest that it can be recommended as a valuable treatment option in clinical practice.

The comparative efficacy and safety of small molecule drugs versus adalimumab and its biosimilars in plaque psoriasis remain insufficiently characterized. This systematic review and network meta-analysis, conducted in accordance with PRISMA guidelines, synthesized evidence from PubMed, Web of Science, and Embase, including 32 studies with a total of 14,622 patients across 30 treatment regimens. A Bayesian random-effects network meta-analysis was conducted using the GeMTC package in R to evaluate primary outcomes (PASI-75 and PGA 0/1) and secondary outcomes (PASI-90, PASI-100, and DLQI 0/1). Safety was assessed by adverse event incidence and treatment discontinuation rates. Results showed that HLX03 had the highest probability of achieving PASI-75 (86.6

BackgroundIn previous studies, the systemic inflammatory response index (SIRI) might be a predictor for chronic inflammation, but the relationship between SIRI and eczema continues to be ambiguous. The objective of the study was to clarify the connection between the level of SIRI and eczema prevalence among children and adolescents.MethodsThe National Health and Nutrition Examination Survey (NHANES) was the database from which we accessed information, comprising participants aged 3–19 years. Furthermore, the investigation of the association between SIRI and eczema was carried out by using logistic regression, and restricted cubic spline models were used to explore nonlinear relationships.ResultsA total of 3,397 subjects, featuring a median age of 11.97 ± 4.87 years, were selected, and 368 (10.83%) were diagnosed with eczema among these participants. Statistically significant differences were observed in the baseline SIRI characteristics for age, race, and BMI quartiles (p < 0.001). In adjusted logistic regression models, the negative association between SIRI and eczema was indicated (OR: 0.83; 95% CI: 0.69–1.00, p < 0.05), suggesting that a one-unit increase in SIRI corresponds to a 17.17% decline in the odds of eczema prevalence. Meanwhile, a nonlinear relationship was revealed by the restricted cubic spline (RCS) between SIRI and eczema prevalence among children and adolescents. The findings of subgroup analysis suggested that there were no significant effects of any covariates on this relationship (all p for interaction > 0.05).ConclusionThe association between SIRI and eczema prevalence in children and adolescents is negative, indicating that elevated SIRI exhibits a protective effect against eczema in children and adolescents, whereas those with low SIRI may require closer monitoring for eczema development.

ABSTRACT Aims This review aimed to investigate whether atopic dermatitis (AD) increases the risk of inflammatory bowel disease (IBD) by analyzing data from longitudinal studies. Methods Cohort and case–control studies evaluating the association between AD and the risk of IBD, Crohn's disease (CD), or ulcerative colitis (UC) were included. Literature searches were conducted in PubMed, CENTRAL, Embase, Scopus, and Web of Science databases up to April 15, 2024. Results A total of eight retrospective cohort studies comprising 61 190 816 participants were included. Meta‐analysis revealed that AD significantly increased the risk of IBD (OR: 1.37, 95% CI: 1.31–1.43) without statistical heterogeneity. Further pooled analysis showed that AD was a significant risk factor for CD (OR: 1.51, 95% CI: 1.31–1.76) and UC (OR: 1.33, 95% CI: 1.13–1.56), with high inter‐study heterogeneity (I2 = 83% and 89%, respectively). Sensitivity analyses confirmed the robustness of the results. Conclusion AD is associated with an increased risk of IBD, significantly elevating the risk of both CD and UC.

BACKGROUND:Psoriasis is a prevalent cutaneous inflammatory disorder characterized by elevated keratinocyte inflammation. 5(S)-6(R)-7-trihydroxyheptanoic-acid-methyl-ester (BML-111), an established analogue of lipoxin A4, is known for its potent anti-inflammatory properties. However, the precise role of BML-111 within a murine psoriasis-like dermatitis model requires further clarification. This research aims to investigate the modulatory effects of BML-111 on inflammatory responses, the p38/mitogen-activated protein kinase (MAPK) signaling cascade, and T helper type 1 (Th1), Th2, and Th17 cell responses within the context of a murine psoriasis-like dermatitis model. METHODS:A psoriasis-like dermatitis model was established by applying 5% imiquimod (IMQ) cream to the backs of C57BL/6 mice, which were pretreated intraperitoneally with or without BML-111 prior to IMQ application. Hematoxylin-eosin staining was utilized to detect the pathological alterations of the murine dorsal skin tissue. Furthermore, the psoriasis area and severity index (PASI) scoring system was used to assess the dynamic cutaneous alterations in the mice. The levels of tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), interleukin (IL)-1β, IL-6, IL-4, and IL-17A in the murine serum samples were quantified by means of enzyme-linked immunosorbent assays (ELISA). Western blotting was conducted to detect the proteins of TNF-α, IL-1β, IL-6, phospho-p38 (p-p38), and p38 in murine skin tissues. Lastly, a flow cytometry analysis was executed to evaluate the expression of peripheral blood Th1/Th2/Th17 cell subsets. RESULTS:BML-111 attenuated IMQ-induced pathological changes in skin tissue of psoriasis-like dermatitis mice. BML-111 treatment substantially reduced TNF-α, IL-1β, IL-6, IFN-γ and IL-17A levels and elevated IL-4 levels in serum and skin lesion tissues of IMQ-induced mice (p < 0.01, p < 0.01, p < 0.01, p < 0.05, p < 0.05, p < 0.05, respectively). The ratio of Th1/Th17 cells in the peripheral blood of BML-111-treated mice was substantially diminished and the ratio of Th2 cells was substantially augmented (p < 0.05, p < 0.01, p < 0.001, respectively). Mechanistically, p-p38 protein level was substantially reduced in the skin tissues of BML-111-treated mice (p < 0.05). While, dehydrocorydaline (DHC, a p38/MAPK pathway agonists) reversed the reduction of p-p38 protein level induced by BML-111 treatment in psoriasis-like mice (p < 0.05). CONCLUSION:BML-111 modulates the p38/MAPK signaling pathway and Th1/Th2/Th17 cytokine response, and alleviates psoriasis-like dermatitis in mice.

We aimed to explore the effects of silencing NOD-like receptor protein 3 (NLRP3) on proliferation of psoriasis-like HaCaT cells and expressions of cytokines. HaCaT cells were treated with human keratinocyte growth factor (KGF) and were divided into KGF group, negative control group, NLRP3-RNAi group and control group. Cells proliferation was detected by CCK8, cell clone formation rate was detected by clone formation assay, distribution of cells cycle was detected by flow cytometry, expressions of cyclin B1 (Cyclin B1), cyclin-dependent kinase 2 (CDK2), Ki67 and proliferating cell nuclear antigen (PCNA) proteins were detected by Western blot, and levels of interleukin (IL)-17, IL-23, IL-6 and tumor necrosis factor α (TNF-α) were detected by enzyme-linked immunosorbent assay. Compared with control group, expressions of NLRP3 mRNA and protein, proliferation rate and clonal formation rate were increased in KGF group, percentage of cells in G0/G1 phase was decreased, percentage of cells in S phase was increased, expressions of Cyclin B1, CDK2, Ki67 and PCNA proteins were increased, and levels of IL-17, IL-23, IL-6 and TNF-α were increased. Compared with negative control group, expressions of NLRP3 mRNA and protein, proliferation rate and clonal formation rate were decreased in NLRP3-RNAi group, percentage of cells in G0/G1 phase was increased, percentage of cells in S phase was decreased, expressions of Cyclin B1, CDK2, Ki67 and PCNA proteins were decreased, and levels of IL-17, IL-23, IL-6 and TNF-α were decreased. Silencing NLRP3 gene can inhibit the proliferation of psoriasis-like HaCaT cells, arrest cell cycle, inhibit the expressions of cell proliferation-related proteins and reduce levels of pro-inflammatory factors.

ObjectiveThe aim of this study was to investigate the role and mechanisms of miR-155 in chronic spontaneous urticaria (CSU).MethodsThe expression level of miR-155 in the skin tissues of patients with CSU and experimental rats were detected by RT-qPCR, followed by the measurement of the histamine release rate in the serum through the histamine release test. Besides, hematoxylin & eosin staining was used to observe the pathological changes of the skin tissues; Corresponding detection kits and flow cytometry to measure the changes of immunoglobulins, inflammatory cytokines and T cell subsets in the serum of rats in each group; and western blot to check the expression level of proteins related to JAK/STAT signaling pathway in the skin tissues.ResultsKnockdown of miR-155 reduced the number and duration of pruritus, alleviated the skin damage, and decreased the number of eosinophils in CSU rats. Moreover, knockdown of miR-155 elevated the serum levels of IgG and IgM, decreased the levels of IgA and inflammatory cytokines, and reduced the proportion of CD4 + and CD4 + CD25 + T cells, as well as the CD4+/CD8 + ratio in CSU rats. However, Tyr705 intervention could reverse the effects of knockdown of miR-155 on CSU model rats. Furthermore, we found that knockdown of miR-155 significantly reduced the protein expression of IRF-9, as well as the P-JAK2/JAK2 and P-STAT3/STAT3 ratios in the skin tissues of CSU rats.ConclusionKnockdown of miR-155 can alleviate skin damage and inflammatory responses and relieve autoimmunity in CSU rats by inhibiting the JAK/STAT3 signaling pathway.

目的 探讨蜈蚣败毒饮联合中药封包对寻常性银屑病的临床疗效及对血清炎性因子的影响.方法 将69例寻常性银屑病(血瘀证)患者随机分为治疗组35例和对照组34例.治疗组予以蜈蚣败毒饮联合全蝎膏封包治疗,对照组仅予以全蝎膏封包治疗,治疗4周观察PASI评分、中医证候评分、血清炎性因子IL-6、IL-22、TNF-α、IFN-γ水平变化.结果 两组患者治疗后PASI评分、中医证候评分、IL-6、IL-22、TNF-α、IFN-γ水平较治疗前均显著下降,且治疗组明显低于对照组,差异有统计学意义(P＜0.05).结论 蜈蚣败毒饮联合全蝎膏封包治疗可明显改善寻常性银屑病(血瘀证)患者皮损情况及相关症状,并降低炎症反应,内外结合,疗效突出.

目的:探讨柴胡牡蛎汤加味治疗带状疱疹急性期肝经郁热证患者的疗效以及对患者血清白细胞介素(IL)-6与IL-8水平的影响.方法:选择状疱疹急性期肝经郁热证患者82例,根据随机数字表法分入对照组与治疗组,均选入41例.对照组予阿昔洛韦片;治疗组阿昔洛韦用法同对照组,并予柴胡牡蛎汤加味内服.两组治疗10 d.比较两组疼痛评分、主要症状消退时间、治疗效果以及血清IL-6与IL-8水平.结果:治疗10 d后,两组疼痛视觉模拟量表(VAS)评分明显减少,并且治疗组VAS评分减少更加显著(P＜0.05);治疗组患者的止疱、疼痛缓解、结痂、脱痂的消退时间较对照组均显著缩短(P＜0.05);治疗组与对照组的总有效率对应92.68％、73.17％,差异有统计学意义(P＜0.05);治疗10 d后,两组患者血清IL-6与IL-8水平显著下调,且治疗组下调更明显(P＜0.05).结论:柴胡牡蛎汤加味治疗带状疱疹急性期肝经郁热证的疗效确切,可有效减轻患者的疼痛,缩短主要症状恢复时间,降低血清IL-6、IL-8水平.

带状疱疹是急性疱疹性病毒性皮肤病,严重影响患者健康及生活质量.杨素清教授依据皮损特点和发病过程,认为火、热、湿、毒、瘀是主要的致病因素,将其作为切入点进行分期论治.提出初期由火热妄动,外溢肌肤所致,以火热证多见,投以龙胆泻肝汤清热泻火;中期湿浊内生,流溢肌肤而发,常见于湿毒证,以胃苓汤以利水化湿;后期毒瘀走窜,漫溢肌肤而致,以毒瘀证为主,以桃红四物汤以解毒散瘀.各期随症加减,动态用药.杨素清教授认为疼痛是其治疗的关键所在,临床上常用香附、延胡索,桃仁、红花等止痛对药以行气活血;巧用忍冬藤、鸡血藤、夜交藤,全蝎、蜈蚣、地龙等藤虫类止痛角药以活血通络止痛,将治痛贯穿整个治疗过程.杨素清教授重视安神怡情,喜用柴胡、枳壳等疏肝理气;善用花类之凌霄花、玫瑰花等行气活血止痛;多用珍珠母、磁石等镇静安神.临床常配合火针、中药外涂等外治法,使内外结合,双管齐下,收效颇佳.

Objective:To explore the value of Jiawei Simiao Yong'an ointment in treating radiation dermatitis based on the method of"clearing away heat and toxic materials".Methods:100 patients with radiation dermatitis in our hospital from August 2022 to June 2023 were included as the research object,and the patients were randomly divid-ed into control group and research group,with 50 cases in each group.The control group was treated with routine western medicine,while the research group was treated with Jiawei Simiao Yong'an Ointment on the basis of the control group.After treatment,the clinical efficacy,TCM symptom score,inflammation index and skin lesion heal-ing time of the two groups were compared.Results:At the end of treatment,the total effective rate of the study group was 90.00%,which was higher than that of the control group(74.00%)(P＜0.05).At the end of treat-ment,the scores of TCM symptoms of skin erythema,itching,ulcer,swelling and pain in the study group were lower than those in the control group(P＜0.05).At the end of treatment,the levels of TNF-αand IL-6 in the study group were lower than those in the control group(P＜0.05).After treatment,the healing time of grade 1～2 skin lesions was shorter than that of grade 3,and the study group was shorter than the control group(P＜0.05).Conclusion:Jiawei Simiao Yong'an Ointment based on the method of"clearing heat and detoxicating"can effective-ly improve the clinical efficacy,relieve the severity of TCM symptoms,inhibit the inflammatory reaction of patients and shorten the healing time of skin lesions.

苦参为临床常用中药,具有清热燥湿、杀虫利尿功效.苦参的化学成分复杂,并且具有多种药理作用.该文对近年来苦参的化学成分以及药理作用进行综述,发现苦参的化学成分主要为氧化苦参碱、苦参碱以及黄酮类化合物,具有抗菌、抗病毒、降血糖、降血脂、抗氧化、抗炎、镇静、镇痛、抗肿瘤、免疫调节、保护心脏、抗生育等作用,为苦参的开发及临床应用提供理论依据.

银屑病是一种发病机制复杂、多病因的炎症性、增生性皮肤疾病.近年来银屑病的发病率逐年增高,已成为危害患者身心健康的重大疾病之一.中医基于藏象学说,从脏腑辨治的角度认为银屑病的发生与肝、脾、肾三脏关系密切,"肝主情志""脾为后天之本""久病及肾"等中医理论在银屑病的中医辨证和治疗过程中具有指导意义.治疗上以疏肝、健脾、补肾为基本方法,同时灵活搭配凉血、化湿、祛瘀等药物,常取得满意的治疗效果.本文通过查阅国内外相关文献,整理、分析所收集到的资料,从肝、脾、肾三脏讨论银屑病的论治,旨在阐明中医药治疗银屑病的研究进展,为银屑病的治疗研究提供参考和选择.

Objective: To study the regulatory effect of Wugong Baidu Decoction on the key stimulation, transcription, and secretion factors in the follicular helper T cell（Tfh） pathway in psoriasis mouse skin lesions at the gene transcription level.Methods: 30 healthy C57BL/6 mice aged 4-6 weeks in SPF grade were randomly divided into blank group, model group, methotrexate group(3 mg·L -1 ),Wugong Baidu Decoction low-dose group(0.08 g·mL -1 ),medium-dose group(0.16 g·mL -1 ),and high-dose group(0.32 g·mL -1 ),5 rats in each group.Except for the blank group, the mice in other groups were established with psoriasis skin lesion model on the back.Drug intervention was performed after the modeling was completed.Mice in the methotrexate group were intragastrically administered with 3 mg·L -1 methotrexate suspension on days 1-4,and 9 g·L -1 sodium chloride injection on days 5-8 by gavage.The mice in the low, medium, and high dose groups of Wugong Baidu Decoction were intragastrically given different concentrations of Wugong Baidu Decoction solution.Mice in the blank group and the model group were given 9 g·L -1 sodium chloride injection by intragastric administration, with a volume of 5 mL·kg -1 ,twice a day for 8 days.The mouse psoriasis area and severity index（MPASI） scoring method was used to evaluate the skin lesion index of mice, and the change of MPASI score before and after gavage was calculated（△MPASI）.RT-PCR method was used to detect the mRNA expression levels of IL-6,IL-21,Bcl-6,STAT3,CXCR5,ICOS,PD-1,and CD40L.Pearson correlation analysis was used to investigate the correlation between △MPASI and the transcriptional expression of each factor of the Tfh pathway in skin lesion tissue.Results: Compared with the blank group, the skin lesion index and the expression levels of IL-6 mRNA,IL-21 mRNA,Bcl-6 mRNA,STAT3 mRNA,CXCR5 mRNA,ICOS mRNA,and CD40L mRNA in the modeled mice were significantly increased（P＜0.01）,the expression level of PD-1 mRNA was significantly decreased（P＜0.01）.Compared with the model group, the skin lesion index of mice in each administration group was significantly reduced（P＜0.05）,and △MPASI was significantly increased（P＜0.05）.In the methotrexate group and the medium and high dose groups of the Wugong Baidu Decoction groups, the expression level of key factors IL-6 mRNA,IL-21 mRNA,Bcl-6 mRNA,STAT3 mRNA,CXCR5 mRNA,ICOS mRNA,CD40L mRNA in the Tfh cell pathway of mice skin lesions was significantly decreased（P＜0.05）,and the expression level of PD-1 mRNA was significantly increased（P＜0.05）.With Pearson analysis, it is suggested that in the Tfh cell pathway of psoriatic mice skin lesions, the expressions of IL-6 mRNA,IL-21 mRNA,Bcl-6 mRNA,STAT3 mRNA,CXCR5 mRNA,ICOS mRNA,and CD40L mRNA were negatively correlated with △MPASI（P＜0.05）.And the expression of PD-1 mRNA was positively correlated with △MPASI（P＜0.05）.Conclusions: Wugong Baidu Decoction may play a role in the treatment of psoriasis by regulating the transcription level of key factors in the Tfh pathway.

银屑病在中医归属于"白疕"范畴,糖尿病在中医称之为"消渴",临床中银屑病更易伴发糖尿病,使病情错综复杂,以中医药为切入点治疗两者共病具有广阔发展前景.本文从西医角度出发,简述银屑病与糖尿病在现代生物学基础及危险因素方面具有显著相关性,从中医角度理解,通过归纳各医家认识得出湿邪为发病之初,瘀血贯穿始终,后期机体气阴受损,"湿、瘀、虚"为两者共病的关键病因病机的结论,并阐述中医辨证治疗银屑病与糖尿病共病的用药特点,更好地指导临床实践,发挥中医治疗特色.

Objective:To investigate the effects and possible mechanisms of Dihuang decoction on atopic dermatitis(AD)model mice.Methods:Totally 36 female BALB/c mice were randomly divided into blank group,model group,control group,low-dose group of Dihuang decoction(low-dose group),medium-dose group of Dihuang decoction(medium-dose group),and high-dose group of Dihuang decoction(high-dose group).The AD model was induced by repeated stimulation of the dorsal skin with 2,4-dinitrochlorobenzene(DNCB)in all groups except the blank group.The control group,low dose group,medium dose group,and high dose group were given corresponding drugs by gavage,while the blank group and model group were given saline by gavage.Inflammation scores and organ indices(thymus and spleen)were calculated in each group,and the back skin lesions were stained with HE staining and toluidine blue staining to observe the histopathology and mast cell changes.The expression of total immunoglobulin E(IgE),interferon-γ(IFN-γ)and interleukin-4(IL-4)in the serum was detected by ELISA,and correlation analysis was carried out between the expressions of IgE,IFN-γ and IL-4 and the inflammation scores in the back skin lesions.Results:Compared with the blank group,mice in the model group showed edema,erosion,dryness or moss-like changes in the appearance of the skin on the back,and HE staining showed that the skin on the back of the mice was hyperkeratotic,thickened,and infiltrated by inflammatory cells.Compared with the model group,the appearance of the skin on the back of the mice in the low,medium,and high dosage groups showed improvement in edema,erosion,dryness,or moss-like changes,and the condition of hyperkeratotic,thickened,and infiltrated by inflammatory cells of the skin was alleviated.The model group showed higher skin lesion inflammation score,mast cell number,spleen index,serum IgE,and serum IL-4 than blank group(P＜0.05),while lower serum IFN-γ than blank group(P＜0.05).The low,medium and high dose groups showed lower skin lesion inflammation score,mast cell number,spleen index,serum IgE and serum IL-4 than model group(P＜0.05),while higher serum IFN-γ than model group(P＜0.05).The serum IgE and IL-4 were positively correlated with the score of inflammation degree of skin lesions(P＜0.05),while the serum IFN-γ was negatively correlated with the score of inflammation degree of skin lesions(P＜0.05).Conclusion:Dihuang decoction may play a therapeutic role by alleviating symptoms in AD mice by reducing mast cell infiltration and shifting the immune environment toward Th2-type cells.

目的 研究蜈蚣败毒饮对银屑病大鼠皮损组织辅助性T细胞(Th)9主导通路中关键刺激因子、转录因子、分泌因子的调节作用及机制.方法 将36只SD雄性大鼠分为空白组、模型组、西药组和中药低、中、高剂量组,每组6只,采用甲氨蝶呤诱导银屑病大鼠模型,给药组分别灌胃相应药液,连续8 d.采用改良的银屑病皮损面积和严重程度指数(MPASI)评分法对大鼠皮损指数进行评价,RT-PCR、Western blot、免疫组化染色检测皮损组织转化生长因子-β(TGF-β)、干扰素调节因子4(IRF4)、白细胞介素-9(IL-9)mRNA、蛋白表达及分布.采用线性回归分析法评价除空白组外的大鼠MPASI评分与关键因子间的相关性.结果 与空白组比较,模型组大鼠MPASI评分显著升高,皮损组织TGF-β、IRF4、IL-9 mRNA表达显著升高(P<0.01),TGF-β、IRF4、IL-9蛋白表达显著升高(P<0.01),且主要表达于细胞核及细胞质;与模型组比较,各给药组大鼠MPASI评分均显著降低(P<0.05,P<0.01),皮损组织TGF-β、IRF4、IL-9 mRNA表达显著降低(P<0.05,P<0.01),TGF-β、IRF4、IL-9蛋白表达显著降低(P<0.05,P<0.01).相关性分析结果显示,MPASI评分与皮损组织TGF-β、IRF4、IL-9 mRNA及蛋白表达呈正相关(P<0.05).结论 蜈蚣败毒饮可能通过调控Th9主导通路TGF-β/IRF4/IL-9发挥治疗银屑病作用.