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Introduction: Results from recent trials assessing the effect of oral vitamin C supplementation on serum uric acid (SUA) have been inconsistent., Objectives: The purpose of this study was to explore the association between oral vitamin C supplementation and serum uric acid., Methods: PUBMED, EMBASE, CNKI, Web of Science, and CENTRAL of Cochrane library databases were searched to identify relevant articles published up to February 2020. Heterogeneity was evaluated using I-square (I 2 ) statistics. Random-effects model was used to pool weighted mean differences (WMD) and 95 % confidence interval (CI) as summary effect sizes., Results: The total sixteen eligible randomized controlled trials (RCTs) containing 1,013 participants were included in this meta-analysis. The pooled findings showed that vitamin C supplementation had a significant effect of lowering SUA. The subgroup analyses showed that the effect of vitamin C supplementation on SUA has positive association with mean age of participants <65 years old, the use of placebo or blank control, duration of trials <1 month and high-quality studies. In addition, sensitivity analysis showed that the results of this study were stable. Both Egger's test and Begg's test demonstrated that no evidence of significant publication bias., Conclusions: The results of present meta-analysis have demonstrated that vitamin C supplementation could make a reduction of SUA. The use of placebo, duration of intervention, age of the subjects and study quality have an impact on the effect of oral vitamin C, but the baseline of SUA not., (Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background: C1q/TNF-related protein 1 (CTRP-1), a novel adipocyte factor, may participate in the mechanisms of metabolism and inflammation. Interleukin 6 (IL-6) is a proinflammatory cytokine that is correlated with the severity of coronary heart disease (CHD). In this study, we focused on the levels of CTRP-1 and IL-6 in patients with CHD., Methods: Circulating CTRP-1 and IL-6 levels were measured using enzyme-linked immunosorbent assay in 81 patients with acute coronary syndrome (n=41) or stable angina pectoris (n=40). CTRP-1 and IL-6 levels were also examined in 30 healthy individuals (control group). We examined the correlations between the levels of CTRP-1 and IL-6 and cardiac risk factors in CHD. Logistic regression analysis was performed to screen for factors that predict CHD., Results: Both CTRP-1 and IL-6 concentrations were increased in the acute coronary syndrome or stable angina pectoris group compared with the control group (P<0.01). Both plasma levels of CTRP-1 and IL-6 in the single-, double- and triple-vessel lesion group were higher compared with the control group (P<0.01). CTRP-1 levels were positively correlated with IL-6 (r=0.667, P<0.01) and high-sensitivity C-reactive protein levels (r=0.520, P<0.01) and negatively correlated with HDL-C (r=-0.432, P<0.01). The logistic regression analysis showed that increases in CTRP-1 and IL-6 levels may be powerful predictors of CHD., Conclusions: The variation of plasma CTRP-1 and IL-6 concentrations may play an important role in reflecting the degree of inflammation in CHD and the severity of coronary arterial atherosclerosis. This potential suggests that evaluating CTRP-1 and IL-6 in combination may aid in predicting the occurrence of CHD.

PSGL-1, the optimal selectin ligand demonstrated by in vivo studies to date, is an essential adhesive molecule mediating the rolling of leukocytes on the endothelial cells and the recruitment of leukocytes to the inflamed tissue. Recent studies demonstrated, in addition to its direct role in capture of leukocytes from the bloodstream, PSGL-1 also functions as a signal-transducing receptor and initiates a series of intracellular signal events during the activation of leukocytes. Our present work showed antibody engagement of PSGL-1 upregulated the transcriptional activity of CSF-1 promotor and increased the endogenous expression of CSF-1 mRNA in Jurkat cell. Overexpression of wild-typed non-receptor tyrosine kinase Syk, but not kinase dead mutant of Syk, promoted the upregulation of the transcriptional activity of CSF-1 promoter caused by antibody engagement of PSGL-1. Additionally, special inhibitor of Syk Piceatannol suppressed the increase of CSF-1 mRNA caused by the engagement of PSGL-1. The results suggest that signal transducted by PSGL-1 upregulate the transcriptional activity of CSF-1, and non-receptor tyrosine kinase Syk participates in this pathway.