Increased plasma/serum levels of prolactin in multiple sclerosis: a meta-analysis.

OBJECTIVES: Prolactin (PRL) is a polypeptide hormone that is known to stimulate humoral and cell mediated immune responses. PRL levels have been investigated in several autoimmune diseases including multiple sclerosis (MS); however, these have yielded different and inconsistent results. This study aims to perform a more precise evaluation on the plasma/serum PRL levels in MS patients, and to explore the available influential factors. METHODS: Research related to plasma/serum PRL levels in MS patients and healthy controls were gathered using PubMed, EMBASE and The Cochrane Library database (until Mar 31 2016). Pooled standard mean difference (SMD) with 95% confidence interval (CI) was calculated by fixed-effects or random-effect model analysis. Heterogeneity test was performed by the Q statistic and quantified using I2, and publication bias was evaluated using a funnel plot and Egger's linear regression test. RESULTS: 516 articles were obtained after searching databases, and 8 studies with 426 MS patients and 296 controls were finally included. Meta-analysis revealed that, compared with the control group, the MS group had significantly higher plasma/serum PRL levels, with the SMD of 0.55 and 95%CI (0.39, 0.72). Subgroup analyses showed that region, age and disease duration were associated with PRL level in MS patients. CONCLUSION: In summary, our meta-analysis revealed a significantly higher PRL level in MS patients than healthy controls, and it is influenced by region, age and disease duration.

[Based on the low-density cDNA Macroarray for screening of antiviral proteins of IFNa tissues].

OBJECTIVE: To screen the gene expression profiles of IFN-alpha antiviral proteins based on a low-density cDNA Macroarray, and to explore the relationship between the expression of antiviral protein and the HBV replication. METHODS: The HepG2 and HepG2.2.15 cells were treated with various concentrations of IFN-alpha (0 IU/ml, 100 IU/ml, 1000 IU/ml) of IFN-alpha for 6 h, and then the low-density cDNA Macroarray was used for analysing the expression profiles of antiviral genes and screening differential expressions of antiviral proteins. Meanwhile, the HepG2 cells were transiently transfected with HBV core protein-expressed plasmid pHBc-EGFP, and the expressions of antiviral proteins were analysed by RT-PCR assay. Moreover, the HepG2.2.15 cells were also transfected with the antiviral protein-expressed plasmid pcDNA3.1-Flag-MxA. ELISA was used for analysing the secreted HBV antigens, while dot blot and Southern blot were applied for analysing the extracellular HBV DNA and intracellular replicative intermediate HBV DNA in HepG2.2.15 cells. All data were presented as mean+/-SD and analyzed using the t-test and one-way analysis of variance (ANOVA) in the experiments. RESULTS: The Macroarray results suggested that the expression of IFN-alpha antiviral genes like 6-16, IFITM1, IFITM2, IFITM3 and RING4 in HepG2.2.15 cells were partially inhibited. More importantly, it was found, in this research, the expression of antiviral protein MxA in HepG2.2.15 cells was completely suppressed. RT-PCR analysis indicated that the expression of MxA was also significantly decreased in HepG2 cells transfected with pHBc-EGFP plasmid. Although HepG2.2.15 cells transfected with pcDNA3.1-Flag-MxA plasmid could not inhibit extracellular HBV DNA and intracellular replicative intermediate HBV DNA, the MxA exerted some antiviral activities as it effectively suppressed the secretion of HBsAg and HBeAg in HepG2.2.15 cells. CONCLUSIONS: HBV and its antigen components probably influence the expression of antiviral proteins. IFN- resistance may be related to the down-regulation of antiviral proteins expression.