miR-185-5p alleviates the inflammatory response of acute gouty arthritis by inhibiting of IL-1β / 细胞与分子免疫学杂志

Objective To investigate the relationship between interleukin-1β (IL-1β) and miR-185-5p in the process of joint injury in acute gouty arthritis (AGA). Methods The serum miR-185-5p levels of 89 AGA patients and 91 healthy volunteers were detected by real-time quantitative PCR. The correlation between miR-185-5p expression level and VAS score or IL-1β expression level was evaluated by Pearson correlation coefficient method. Receiver operating characteristic (ROC) curve was used to evaluate the diagnostic value of miR-185-5p in AGA. THP-1 cells were induced by sodium urate (MSU) to construct an in vitro acute gouty inflammatory cell model. After the expression level of miR-185-5p in THP-1 cells was upregulated or downregulated by transfection of miR-185-5p mimics or inhibitors in vitro, inflammatory cytokines of THP-1 cells, such as IL-1β, IL-8 and tumor necrosis factor α (TNF-α), were detected by ELISA. The luciferase reporter gene assay was used to determine the interaction between miR-185-5p and the 3'-UTR of IL-1β. Results Compared with the healthy control group, the expression level of serum miR-185-5p in AGA patients was significantly reduced. The level of serum miR-185-5p was negatively correlated with VAS score and IL-1β expression level. The area under the curve (AUC) was 0.905, the sensitivity was 80.17% and the specificity was 83.52%. Down-regulation of miR-185-5p significantly promoted the expression of IL-1β, IL-8 and tumor necrosis factor (TNF-α), while overexpression of miR-185-5p showed the opposite results. Luciferase reporter gene assay showed that IL-1β was the target gene of miR-185-5p, and miR-185-5p negatively regulated the expression of IL-1β. Conclusion miR-185-5p alleviates the inflammatory response in AGA by inhibiting IL-1β.

The relationship between gene polymorphism and serum expression of interleukin-10 with intracranial aneurysm / 天津医药

Objective To analyze the associations of the interleukin-10 (IL-10) promoter-1082G/A and-819C/T single nucleotide polymorphism (SNP) and serum level of IL-10 with intracranial aneurysm (IAs). Methods The polymerase chain reaction (PCR) and DNA direct sequencing methods were used to detect IL-10 gene promoter district two SNP site,-1082G/A and-819C/T genotype frequency and allele frequency in 206 patients with IAs and 187 controls. Chi-square test was used to analyze differences between two groups. The serum level of IL-10 was analyzed by ELISA, and t-test was used to analyze significant differences between two groups. Results There were significant differences in genotypes of GG and GA+AA, as well as the alleles G and A, in-1082G/A locus between IAs group and control group (P<0.01). There were higher frequencies of genotype GA+AA and the allele A in IAs group than those in control group (P<0.01). There was higher risk of suffering IAs in patients with genotype GA+AA (OR=4.137, 95%CI:2.476-6.914) and the allele A (OR=3.368, 95%CI:2.476-4.583). There were higher frequencies of the genotype CT+TT and the allele T in-819C/T locus in IAs group than those of control group (P<0.01). There was higher risk of suffering IAs in patients with genotype CT+TT (OR=3.393, 95%CI:1.952-5.900) and the allele T (OR=3.764, 95%CI:2.730-5.192). The serum level of IL-10 was significantly lower in IAs group than that of control group (P<0.01). Conclusion The IL-10 promoter SNP influences the expression of IL-10. IL-10 promoter-1082G/A and-819C/T polymorphisms are correlated with the formation of IAs.