Objective This study aimed at exploring the effects of luteolin on psoriasis-like cell model proliferation, apoptosis regulation and the expression of inflammation-related mediators. Methods A Cell Counting Kit-8 (CCK-8) assay was used to determine the survival rate of human immortalized keratinocytes (HaCaT cells) and normal human epidermal keratinocytes (NHEK cells) following stimulation with luteolin and lipopolysaccharide (LPS). Western blot and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis were used to detect the protein and mRNA expressions of nuclear factor (NF)-κB p65 and interleukin (IL)-6 after LPS stimulation. Then a luteolin stimulation protocol (10 μmol/L, 24 h) was determined and a reasonable LPS stimulation concentration (20 μg/mL, 24 h) was chosen to establish the psoriasis cell model. Keratinocytes in luteolin pre-treatment and control groups were stimulated with 20 μg/mL LPS for 24 h, and the expressions of NF-κB p65 and IL-6 were detected by western blot and RT-qPCR. The apoptosis of HaCaT cells was detected by flow cytometry, and the enzyme-linked immunosorbent assay (ELISA) was used to detect the expression of psoriasis-related inflammatory factors. Results CCK-8 assay indicated that luteolin inhibited the proliferation of keratinocytes. LPS stimulated the proliferation of keratinocytes and upregulated the expression of NF-κB p65 and IL-6 in a concentration-dependent manner, and induced psoriasis-like changes. Furthermore, the protein and mRNA expression levels of NF-κB p65 and IL-6 were decreased in the luteolin pre-stimulation group ( p < 0.05). Treatment with luteolin downregulated the expression of the LPS-induced inflammatory mediators in keratinocytes ( p < 0.05). The flow cytometry results showed that luteolin induced HaCaT cells apoptosis. Finally, ELISA results demonstrated that luteolin inhibited the release of the IL-17, IL-23 and tumor necrosis factor α (TNF-α) in the pre-stimulation group ( p < 0.05). Conclusion This study confirmed that luteolin can effectively relieve inflammatory mediators in LPS-induced keratinocyte models of psoriasis, which suggested the potential of luteolin in treating psoriasis.

Herpes zoster (HZ), caused by the varicella-zoster virus, is an infectious skin disease that rarely recurs after initial presentation. The mechanism underlying HZ recurrence is currently under investigation. In this article, we report a case of HZ relapse within 1 month. Analysis of patient’s clinical manifestations, histopathological features, and flow cytometry results indicated that the absolute and percentage values of B cells were below the lower limit. We hypothesized that the patient had abnormal humoral immune function, which may be one reason leading to the HZ relapse within 1 month. The findings of this case will serve as useful reference for HZ recurrence for clinicians. This case was impactful and added to the literature on HZ recurrence.