Background: Several studies have investigated the relationship between psoriasis and adverse cardiovascular outcomes. Previous meta-analyses have shown psoriasis to be a risk factor for adverse cardiovascular outcomes. However, the relationship has become uncertain with the emergence of many new studies.Objective: This study aimed to conduct an updated meta-analysis on cohort studies about the relationship between psoriasis and adverse cardiovascular outcomes.Methods: Electronic databases (accessed till January 2022) were searched systematically for cohort studies assessing the cardiovascular risk in psoriasis patients. This was a meta-analysis using a random-effect model; pooled analyses of several cardiovascular outcomes were also conducted.Results: A total of 31 [hazard ratio (HR), 23; rate ratio (RR), 8] studies involving 665,009 patients with psoriasis and 17,902,757 non-psoriatic control subjects were included for the meta analysis. The pooled analyses according to each cardiovascular outcome revealed that pooled RR of patients for developing myocardial infarction, stroke, cardiovascular death, ischemic heart disease, thromboembolism and arrhythmia were 1.17 (95% confidence interval [CI], 1.11–1.24), 1.19 (95% CI, 1.11–1.27), 1.46 (95% CI, 1.26–1.69), 1.17 (95% CI, 1.02–1.34), 1.36 (95% CI, 1.20–1.55) and 1.35 (95% CI, 1.30–1.40), respectively. Meanwhile, the pooled RR of patients with mild and severe psoriasis for developing adverse cardiovascular outcomes were 1.18 (95% CI, 1.13–1.24) and 1.41 (95% CI, 1.31–1.52), respectively.Conclusion: The pooled analyses revealed that psoriasis is associated with all adverse cardiovascular outcomes of interest, especially in severe patients. Psoriasis remains an independent risk factor for adverse cardiovascular outcomes, which needs more attention from clinicians.

Inhibition of miR-103a-3p suppresses the proliferation in oral squamous cell carcinoma cells via targeting RCAN1

Hepatorenal toxicities are an important side effect of anthracycline antibiotics. The objective of this study was to determine whether sesamin (Ses) protects against acute doxorubicin (DOX)-induced hepatorenal toxicities. Rats received daily treatment with either 0.5% carboxymethylcellulose (10 mL/kg) or Ses (10, 20 and 40 mg/kg) orally for 10 days, followed by an intravenous injection at day 8 of either saline (10 mL/kg) or DOX (20 mg/kg). Hepatorenal toxicity was assessed by measuring the levels of serum creatinine (Cre), blood urea nitrogen (BUN), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP). The protein expression of 4-hydroxynonenal (4-HNE) in hepatorenal tissues was evaluated using immunohistochemistry. The malondialdehyde (MDA) content and antioxidant activity in the kidney and liver tissues were also measured. The results suggest that pretreatment with Ses ameliorated DOX-induced liver and kidney injury by lowering the serum ALT, AST, ALP, Cre and BUN levels ( p < 0.05 or p < 0.01), and the histological damage to the liver and kidney tissues induced by DOX compared to control were also significantly attenuated by Ses. Furthermore, Ses significantly decreased the DOX-induced increase of MDA and 4-HNE and increased the activity of CAT, SOD and GPX compared to the DOX-treated rats ( p < 0.05 or p < 0.01), whereas the change of DOX + Ses (10 mg/kg) group is not significant compared to the DOX-treated group ( p > 0.05). These findings indicate that Ses elicits a typical protective effect against DOX-induced acute hepatorenal toxicity via the suppression of oxidative stress.

It has been reported that zerumbone (ZER) has marked effects on the regulation of cell proliferation and migration in multiple types of cancer, and has anti-cancer effects on various types of malignant cell. However, the effects and underlying molecular mechanisms of treatment with ZER on melanoma cells remain unclear. In the present study, the effect of treatment with ZER on the proliferation, migration and mitochondrial function of the human melanoma cell line CHL-1 was investigated. The results of the present study indicated that treatment with ZER significantly inhibited CHL-1 cell proliferation (P<0.001). Cell migration analysis further demonstrated that ZER inhibited the migration of CHL-1 cells (P<0.001). Treatment with ZER significantly increased cellular reactive oxygen species levels (P<0.001), reduced matrix membrane potential (P<0.001), decreased ATP (P<0.001) and mitochondrial DNA (P<0.001) levels, and decreased mitochondrial transcription factor A mRNA levels (P=0.002). The results of the present study suggested that the inhibition of proliferation and migration was mediated by altered mitochondrial function. In conclusion, the results of the present study suggested that ZER has chemotherapeutic effects on human melanoma cells by altering mitochondrial function.

Lichen amyloidosis (LA) is a chronic, severely pruritic skin disease, which is the most common form of primary cutaneous amyloidosis. The treatment of LA has been considered to be difficult. LA may be associated with atopic dermatitis (AD), and in this setting, the treatment options may be more limited. Herein, we report four cases of LA associated with AD successfully treated by dupilumab. In this article, we describe four cases of patients who presented with recurrent skin rash accompanied by severe generalized intractable pruritus, diagnosed with refractory LA coexisting with chronic AD. Previous treatments had not produced any apparent improvement. Thus, we administered dupilumab injection subcutaneously at a dose of 600 mg for the first time and 300 mg every 2 wk thereafter. Their lesions all markedly improved. Dupilumab may be a new useful treatment for LA coexisting with AD.

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.