Combination of Uric Acid and Pro-Inflammatory Cytokines in Discriminating Patients with Gout from Healthy Controls.

OBJECTIVE: The aim of present study was to explore whether the combination of serum uric acid and pro-inflammatory cytokines could improve the accuracy of diagnosis of gout. METHODS: A total of 94 patients with gout were selected as the patient group, and 52 healthy subjects were selected as the control group. Serum levels of uric acid and pro-inflammatory cytokines (C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α)) were measured in both groups. Correlation between serum uric acid and pro-inflammatory cytokines was assessed using Pearson correlation analysis. The area under curve (AUC) of CRP, IL-6, TNF-α combined with uric acid for the diagnosis of gout were evaluated by receiver operating characteristic (ROC) curve method. RESULTS: Compared with the control group, the levels of serum uric acid, CRP, TNF-α and IL-6 were significantly increased in the patients. Moreover, there was a positive correlation between serum uric acid and CRP (r = 0.179, P = 0.033), IL-6 (r = 0.194, P = 0.039), and TNF-α (r = 0.496, P < 0.001) levels. Furthermore, the AUCs of CRP, IL-6, TNF-α combined with uric acid level for the diagnosis of gout were 0.932, 0.884, and 0.972, respectively. Additionally, the AUC for the combination of uric acid, CRP, and TNF-α was 0.982 in discriminating patients with gout from healthy volunteers. CONCLUSION: The combination of serum uric acid and pro-inflammatory cytokines could improve the accuracy of diagnosis of gout.

Kruppel like factor 10 up-regulates PDZ and LIM domain containing protein 2 via nuclear factor kappa-B pathway to inhibit proliferation and inflammatory of fibroblastoid synovial cell in rheumatoid arthritis.

Rheumatoid arthritis (RA) is an autoimmune disease caused by synovitis. Two genes, KLF10 (Kruppel like factor 10) and PDZ and LIM domain containing protein 2 (PDLIM2), play key roles in cell inflammation and proliferation. However, the specific roles of the two on inflammation and proliferation of RA-fibroblastoid synovial cell (RA-FLS) have not been reported so far. RT-qPCR and Western blot detected the expressions of PDLIM2 and KLF10 in Human Rheumatoid arthritis FLSs (HFLSs-RA). Cell transfection techniques overexpressed PDLIM2 and KLF10 or inhibited the expression of KLF10. JAPAR database predicted the binding sites of PDLIM2 and KLF10, and the binding between the two was detected and verified using luciferase reporter genes and ChIP. Subsequently, CCK-8 technology, TUNEL staining, Western blot, wound healing and ELISA detected proliferation-related indicators, migration-related indications and inflammation-related indicators. Finally, western blot was used to detect the expression of NF-κB pathway-related proteins to further explore the mechanism.The expression of PDLIM2 was decreased in HFLSs-RA. Overexpression of PDLIM2 inhibited proliferation, migration and inflammation in HFLSs-RA. KLF10 can transcriptionally activate PDLIM2. Interfering with KLF10 reversed the inhibition effects of PDLIM2 overexpression on the proliferation, migration and inflammation, which was possibly through the NF-κB pathway. Overall, KLF10 can up-regulate PDLIM2 by regulating the NF-κB pathway to inhibit inflammation and proliferation of HFLSs-RA.