Objective To investigate the effects of paeoniflorin on imiquimod-induced psoriasis in a mouse model and the underlying mechanisms. Methods Fifteen healthy BALB/C mice were randomly divided into the control, model, and model group-treated with low-, medium-, and high- doses of paeoniflorin, once daily for 7 days. The back skin of mice in the control and model groups were treated topically with Vaseline and imiquimod ointment, respectively. The imiquimod-treated mice were intragastrically given either saline or paeoniflorin at doses of 75 mg/(kg·d), 150 mg/(kg·d) and 300 mg/(kg·d), twice daily. The erythema and scaling on the treated area of the skin were observed. The skin biopsies were obtained from the treated area for H&E staining to observe the changes in histopathology and the skin thickness of the lesions, while immunofluorescence was applied to detect neutrophil infiltration. The expression levels of TNF-α and IL-17 mRNA were assessed with RT-PCR. In addition, Western blot was used to assess the expression of citrullinated histone 3 (CitH3). Results Compared with the model group, topical treatment with paeoniflorin attenuated multiple changes in the imiquimod-treated skin, including reduced erythema and scaling, decreased epidermal thickness and neutrophil infiltration, down-regulation of TNF-α and IL-17 mRNA expression (P<0.001 vs. imiquimod alone for all) in addition to reduction in expression levels of CitH3 (all P<0.05 vs. imiquimod alone).Moreover, paeoniflorin-induced changes in expression levels of IL-17 and CitH3 were dose-dependent (P<0.05 for both). Conclusion Paeoniflorin can modulate neutrophil extracellular traps, resulting in down-regulation of the expression levels of inflammatory cytokines, consequently alleviating cutaneous inflammation in a mouse model of psoriasis.

Objective To evaluate the clinical efficacy of elevation combined with suspension technique in the treatment of boxcar acne scars. Methods This split-face self-controlled study included 7 patients with boxcar acne scars who were treated at the Dermatology Hospital of Southern Medical University between January and May 2024. One side of patients' face received only elevation treatment (the elevation group), while the other side received elevation surgery followed by suspension surgery (the combined group). The extent of improvement in scar was compared between the two groups one month after the treatment. Results At baseline, neither patient self-assessment scores of VAS nor physician assessment scores differed significantly between the two groups (VAS: 8.54±0.76 vs. 8.36±0.57, t=-0.52, P=0.614; physician assessment scores: 8.39±0.99 vs. 7.96±0.54, t=-1.00, P=0.336). One month after the treatment, more significant reductions in both patient self-assessment scores of VAS and physician assessment scores were observed in the group of combination therapy than in that of elevation alone (VAS: 6.21±1.01 vs. 3.40±0.69, t=5.97, P=0.001; physician assessment scores: 5.96±1.16 vs. 3.40±0.96, t=4.69, P=0.003). Moreover, both patient self-assessed efficacy and physician-evaluated efficacy were higher in the combination group than in the elevation group (both P<0.01). No significant adverse reactions were observed in either group. Conclusion Although either combination of elevation and suspension methods or elevation alone is effective for boxcar acne scars, the former displays superior efficacy.

Objective To investigate the serum levels of soluble suppression of tumorigenicity 2 (sST2) and C-C chemokine ligand 19 (CCL19) in patients with psoriasis vulgaris (PV) at the progressive stage and their clinical significance. Methods From January 2021 to June 2023, 86 psoriatic patients at the progressive stage were enrolled. The patients were divided into mild, moderate, and severe groups according to the severity of disease. A total of 86 healthy individuals who underwent routine physical examination were enrolled during the same period. Enzyme linked immunosorbent assay (ELISA) was applied to detect the levels of sST2, CCL19, interleukin-17A, IL-21, IL-22, and IL-23 in the serum of both groups. Pearson and Spearman's methods were used to analyze the correlation of serum levels of sST2 and CCL19 with inflammatory cytokines and psoriasis area and severity index (PASI), respectively. The influencing factors of PV were analyzed using multivariate logistic regression. ROC curve was plotted to analyze the diagnostic value of serum levels of sST2 and CCL19 for PV. Results The serum levels of sST2, CCL19, IL-17A, IL-21, IL-22, and IL-23 in the study group were significantly higher than that in the control group (P<0.05). The serum levels of sST2, CCL19, IL-17A, IL-21, IL-22, and IL-23 were positively associated with disease severity (P<0.05). Pearson's correlation analysis showed that the serum level of sST2 was positively correlated with CCL19 (P<0.05), and both sST2 and CCL19 levels were positively correlated with the levels of IL-17A, IL-21, IL-22, and IL-23 (P<0.05). Moreover, Spearman's correlation indicated that the serum levels of sST2 and CCL19 were positively correlated with PASI (P<0.05). Multivariate logistic regression analysis revealed that the serum levels of sST2 and CCL19 were risk factors for PV (P<0.05). According to the ROC curve, the combination of serum levels of sST2 and CCL19 was superior to individual marker in the diagnosis of PV (Z=2.71, Z=2.70, P<0.05). Conclusions The serum levels of sST2 and CCL19 are greatly elevated in patients with PV at the progressive stage, and the combination of these two biomarkers can be helpful in the diagnosis of PV at the progressive stage.

Objective To report a family with hereditary angioedema (HAE) and to conduct their genetic mutation analysis. Methods Clinical data of the HAE family were collected, and DNA was extracted from the peripheral blood of the family members. The exon coding region of serine protease inhibitor G1(SERPING1) gene of the proband and family members was directly sequenced by Sanger sequencing technology. Results The family had a total of 16 people for three consecutive generations, with 9 patients suffering from HAE. All the 9 patients showed repeated erythema, edema and pruritus of the whole-body skin, among which 3 patients died of acute attack. Genetic sequencing was conducted in all 13 individuals. A heterozygous mutation in SERPING1 gene c.1396C>G (p.Arg466Gly) was detected in all the 6 HAE patients, while no gene mutation was found in the 7 healthy person. Conclusion The heterozygous mutation of c.1396C>G in the SERPING1 gene might be the cause of hereditary angioedema in this family.

Objective To investigate the characteristics of lesions and clinical features of keloids. Methods This study included a total of 395 patients with keloids who were diagnosed and treated at the Dermatology Department of the Second Hospital of Hebei Medical University between October 2022 and October 2023. Patients' general information, characteristics of onset and treatment history were analyzed. Results The male-to-female ratio was 1 ∶1.04. The peak onset age was between 19~28 years old. The chest (48.35%) and shoulders/back (22.28%) were the two most commonly affected areas. One hundred sixty-two (41.01%) patients had single lesion on single site. Patients with a family history of keloids accounted for 4.30%. Among the 395 patients, 74.94% of the patients had not received any treatments, while 25.06% had a history of treatment prior to visiting our clinic. Twelve patients had received multiple or combination modality treatments, and 87 patients had received single modality treatment. Patients who had received previous treatments experienced recurrence. Conclusions Keloids primarily affect young individuals, predominantly on the chest and shoulders/back, and mostly present as single lesion on one body site. There are no significant differences in onset sites, clinical classification and lesion sizes between genders. Genetic factors can affect the development of keloids. Patients with keloids are often treated with local drug injection, surgical resection, and other methods. But the recurrence rate is high, indicating a challenge in the treatment of keloids.

Objective To explore the mechanisms whereby Buyang Huanwu Decoction (BYHWT) imoroves peripheral neuropathic pain (PNP) through network pharmacology and molecular docking. Methods The active ingredients and targets of BYHWT were screened through the ETCM and SwissTargetPrediction databases. Peripheral neuropathic pain-related targets were screened through the GeneCards, OMIM, TTD, and DisGeNET databases. The venn diagram of intersection targets was plotted using the ggvenn package in R. The ″formulated drugs-active ingredients-disease targets″ network was constructed using Cytoscape software. The protein-protein interaction (PPI) network was established using the STRING database. Gene ontology (GO) enrichment analysis and kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analysis were performed using the clusterProfiler package in R. Molecular docking of core active ingredients and core targets was conducted using the AutoDock software. Results A total of 257 active ingredients and 844 affected targets were screened, along with 3 143 peripheral neuropathic pain-related targets and 478 intersection targets. The PPI analysis revealed core targets, including protein kinase Src (SRC), signal transducer and activator of transcription 3 (STAT3), protein kinase B (AKT1), and epidermal growth factor receptor (EGFR). The GO enrichment analysis identified 3 659 GO terms, encompassing 3 206 biological process, 143 cellular component and 310 molecular functions. KEGG enrichment analysis identified 303 signaling pathways, including EGFR tyrosine kinase inhibitor resistance, the AGE-RAGE signaling pathway in diabetic complications, the HIF-1 signaling pathway, and the PI3K-Akt signaling pathway. Conclusions Using network pharmacology and molecular docking techniques, the present study reveals that BYHWT ameliorates peripheral neuropathic pain by multiple ingredients, regulating multiple targets and signaling pathways.

Objective To explore the clinical characteristics and epidemiological status of tinea nigra, and review related literature to improve clinicians' understanding of the disease. Methods Clinical data of an adult patient with tinea nigra was summarized, and the results of mycological dermoscopic examination and molecular identification were presented. In addition, the literature related to tinea nigra was reviewed. Results A brown patch was seen on the right palm. Dermoscopy showed fine dotted and filamentous structures under a brown background. Microscopic examination showed sporulating hyphae and conidia with thick walls. The fungi were identified as Hortaea werneckii by molecular technique. A total of 31 cases of tinea nigra in 19 publications (including this case with a total of 32 cases) were reported in China and 54 papers (105 cases) outside of China. Conclusions Tinea nigra mainly occurs on the palms of children in coastal areas. Non-invasive dermoscopy and fluorescence microscopy can be primary approaches to examine fungal infection, and the pathogenic fungi can be identified by molecular approach. It can be easily misdiagnosed as malignant melanoma. Clinicians should be aware of this disease to avoid unnecessary biopsy or resection.

A case of umbilical pemphigus vulgaris is reported. A 37-year-old female presented with a half-year history of repeated oral blood blisters and periumbilical itchy blisters. Dermatological examination revealed a demarcated annular irregular erosive surface covered with odorless white secretions on the umbilical area. But neither blisters nor erosions were observed in the oral mucosa. PDAI activity scores were 2 points. Pathological examination of skin lesion showed blisters in the basal layer and acantholytic cells in the epidermis, and lymphocytic infiltrations in the superficial dermis. Direct immunofluorescence revealed reticular deposition of IgG and C3 in the intercellular space of the spinous layer, without IgM and IgA depostion. The diagnosis was pemphigus vulgaris. Patient was treated with intramuscular injection of Methotrexate (10 mg) once, and oral methylprednisolone tablets at a dose of 24 mg once daily, in addition to calcium supplementation and topical applications of Halometasone and Sodium Fusidate Ointment. After the skin lesion was improved, the patient was discharged. No new lesions occurred during 6-month phone follow-up.

We report a case of ustekinumab-induced pustular psoriasis treated with IL-17A inhibitor. A 51-year-old female presented with red plaques and scales for 20 years, with aggravation and pustules for over 10 days. The patient was previously diagnosed with plaque psoriasis, and poorly responded to systemic medications. After ruling out contraindications, the patient was subcutaneously given 45 mg of ustekinumab, resulting in clearance of the skin lesion. But erythema and scales with pustules appeared all over the body after the fourth treatment. Physical examination revealed scattered red plaques covered with white-silver scales, and Auspitz sign (+) on the head and face. The trunk and limbs were scattered with large erythematous patches and erythematous plaques, covered with various size of dense pustules, in a target-shape with a brown center. Some pustules merged to pus-lake. Pustules with erosive surface were scattered on the vulvar mucosa. Nails appeared thimble-like with nail plate thickening. Histopathology showed hyperkeratosis, parakeratosis, thinning or disappearance of granular layer, psoriasis-like epidermal hyperplasia, Munro and Kogoj microabscesses, papillary dermal edema, vascular dilation, and perivascular lymphocytic infiltration. Diagnosis was pustular psoriasis. After the treatment with topical corticosteroids and 160 mg of ixekizumab, the rashes subsided within 3 days. Afterwards, patient was treated with ixekizumab according to the manufacturer's instruction, without the development of new lesion during 1-year follow-up.

Skin photoaging, a phenomenon of premature skin aging due to prolonged exposure to ultraviolet (UV) radiation, manifests as wrinkles, loss of skin elasticity, pigmentation disorders, and age spots. Non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), play a crucial role in regulating gene expression and the development of skin photoaging. This review summarizes the molecular mechanisms of specific ncRNAs (such as miR-34a,miR-134,miR-1246,lncRNA H19-miR-296-5p-IGF2, lncRNA PVT1-miR-551b-3p-AQP3,lncRNAMeg3-miR-93-5p-epiregulin,circ-COL3A1-859267 and circ-0011129) in skin photoaging. Additionally, the review discusses the potential application of ncRNA-based therapies in photoaging, as well as the current challenges and future research directions.

Palmoplantar pustulosis (PPP) is a chronic recurrent inflammatory skin disease. Existing therapeutic methods cannot meet the demand by patients. Phosphodiesterase-4 (PDE-4) is a key enzyme involved in the balance of immunocytes. It acts as a downstream mediator in the signaling pathways of a variety of cytokines which are associated with palmoplantar pustulosis and extensively regulate immune responses. Apremilast, as representative of the oral PDE-4 inhibitors, displays superior efficacy in clinical trials against palmoplantar pustulosis. Crisaborole has also been regulate to induce sustained improvement in skin lesions. This article reviews the research progress on PDE-4 inhibitors in treatment of palmoplantar pustulosis.

Acne is a chronic cutaneous inflammatory disorder of the pilosebaceous units, affecting a large number of adolescents and adults worldwide, and its pathogenesis is still unclear. Its pathogenesis is considered to be related to several factors such as increased sebum secretion, abnormal keratosis of pilosebaceous follicular ducts, Cutibacterium acnes infections and dysbiosis of the skin microbiome, inflammation and immune response, etc. There are multiple signaling pathways involved in the pathogenesis. This article reviews the signaling pathways involved in the pathogenesis of acne, and discusses the role of PI3K/Akt/mTORC 1, Wnt/β-catenin, NF-κB, and MAPK signaling pathways in the pathological process of acne, as well as the important roles of IGF-1, androgens, TLR-2, TH17, etc. in acne inflammation.