SummaryBackgroundPsoriasis is a chronic skin disorder that manifests as epidermal keratinocyte hyperplasia.ObjectivesWe examined the effect of oxymatrine treatment on cell proliferation and apoptosis in skin lesions of psoriasis.Patients and methodsPatients with severe plaque psoriasis were treated with oxymatrine or with acitretin. The skin lesions were stained with proliferating cell nuclear antigen (PCNA), Ki‐67 and Bcl‐2, as well as examined by terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labelling (TUNEL). We performed correlations of the Psoriasis Area and Severity Index (PASI) and the proliferation and apoptosis index.ResultsOxymatrine significantly reduced the psoriasis lesions as demonstrated by the reduced PASI score after treatment [6·91; 95% confidence interval (CI) 5·00–8·81, P < 0·001]. In the oxymatrine group, the mitotic index was 26·15 (95% CI 24·80–27·49) before oxymatrine treatment, decreasing to 14·52 (95% CI 13·82–15·25; P < 0·001) after treatment, but remained higher than the normal group (6·24; 95% CI 5·87–6·61, P < 0·001). Oxymatrine also inhibited the proliferation of epidermal cells in the skin lesion as indicated by the reduced proliferation index after treatment (P < 0·01). In addition, oxymatrine treatment reduced cellular apoptosis as shown by increased Bcl‐2 expression and a decrease in TUNEL‐positive cells. The PASI score was positively correlated with mitotic index, proliferation index and apoptotic index (TUNEL), but negatively correlated with Bcl‐2 expression.ConclusionsOxymatrine treatment reduced proliferation but inhibited apoptosis of cells in the skin lesion. The balance between cell proliferation and turnover may contribute to the significant alleviation of psoriasis by oxymatrine. What's already known about this topic? Psoriasis manifests as epidermal keratinocyte hyperplasia with proliferation, keratinocyte maturation and turnover rates.Current drugs for psoriasis may inhibit cell proliferation but could not adjust the balance of cell division, differentiation and apoptosis. What does this study add? We studied the efficacy of oxymatrine in the treatment of psoriasis and analysed the correlation of skin lesions, proliferation and apoptosis index before and after oxymatrine treatment. What is the translational message? Our study has demonstrated that oxymatrine is effective in the treatment of severe plaque psoriasis.It has comparable efficacy with acitretin.Because acitretin treatment was sometimes associated with metabolic abnormalities, our study suggests oxymatrine therapy as an alternative treatment for psoriasis in the context of acitretin allergy or adverse reactions.

Background: The long noncoding RNA, small nucleolar RNA host gene 8 (SNHG8), is upregulated in multiple human cancer types. However, whether SNHG8 is aberrantly expressed in esophageal squamous cell carcinoma (ESCC) and its biological functions have yet to be elucidated. Thus, we aimed to determine the expression status of SNHG8 in ESCC, explore the effects of SNHG8 on the oncogenicity of ESCC, and investigate the potential underlying mechanisms. Methods: SNHG8 expression in ESCC tissues and cell lines was determined via reversetranscription quantitative polymerase chain reaction. The actions of SNHG8 on the malignant characteristics of ESCC were explored using CCK-8 assay, flow-cytometric analysis, Transwell migration and invasion assays, and tumor xenografts in nude mice. Results: SNHG8 expression was significantly higher in ESCC tissues and cell lines. High SNHG8 expression was revealed to closely correlate with primary tumor invasion depth, lymph node metastases, TNM stage, and worse overall survival among patients with ESCC. Functional investigation showed that ablation of SNHG8 notably restricted ESCC cell proliferation, migration, and invasion while inducing apoptosis in vitro and hindered tumor growth in vivo. In the meantime, SNHG8 acted as a molecular sponge of microRNA-411 (miR-411) in ESCC. Furthermore, miR-411 exerted a tumor-suppressive effect on ESCC cells, and karyopherin alpha 2 (KPNA2) turned out to be a direct target gene of miR-411. Restoring KPNA2 expression neutralized the inhibitory effects of miR-411 overexpression on the malignant behaviors of ESCC cells. Moreover, silencing of miR-411 abrogated the influence of SNHG8 downregulation in ESCC cells. Conclusion: SNHG8 may play oncogenic roles in the malignancy of ESCC by sponging miR-411 to increase KPNA2 expression. The SNHG8-miR-411-KPNA2 pathway may be a novel target for the treatment of patients with ESCC and offer potential biomarkers for the diagnosis and prognosis of ESCC.

Treatment with oxymatrine effectively ameliorated severe plaque psoriasis, and was accompanied by only minor adverse effects.

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2020) MiR-616 plays oncogenic role in hepatocellular carcinoma progression through suppressing PTEN expression and activating PI3K/AKT pathway, Artificial Cells, Nanomedicine, and Biotechnology, 48:1, 728-734, ABSTRACT Aims: Given their regulatory roles in gene expression, microRNAs play an important role in tumorigenesis. The current study aimed to explore the function and the related mechanisms of miR-616 in hepatocellular carcinoma (HCC). Methods: The expression of miR-616 was detected using quantitative real-time polymerase chain reaction (qRT-PCR). Chi-square test was applied to estimate the association of miR-616 with clinical characteristics of HCC patients. Cell transfection was performed by Lipofectamine V R 2000. MTT assay was used to detect cell proliferation, whereas cell motility was estimated using Transwell assay. The protein expression was detected using western blot. Results: MiR-616 was significantly up-regulated in HCC tissues and cells (p < .05 for all). Moreover, its elevated expression was positively correlated with lymph node metastasis (p ¼ .008) and TNM stage (p ¼ .012). Knockdown of miR-616 resulted in decreased cell proliferation, migration and invasion. Moreover, the inhibition of miR-616 significantly suppressed PI3K/AKT pathway. The bioinformatics analysis and luciferase reporter assay suggested that PTEN was a targeted gene of miR-616. PTEN had the capacity to reverse the oncogenic function of miR-616 in HCC. Conclusion: MiR-616 activates PI3K/AKT pathway through suppressing PTEN expression, thus promoting the progression of HCC. ARTICLE HISTORY