Gout is considered one of the most painful acute conditions caused by deposition of monosodium urate (MSU) crystals within joints. Recent studies have shown that interleukin (IL)-1β is a key inflammatory mediator in acute gouty arthritis (GA), and its level is regulated by microRNAs (miRNAs). However, the molecular mechanisms of the regulation remain unclear. A miRNA microarray was used to analyze the miRNA expression profiles in peripheral white blood cells (WBCs) of patients with GA. THP-1 cells were transfected with miRNA mimics, stimulated by MSU crystals, and then subjected to quantitative real-time polymerase chain reaction or Western blot analysis. Levels of IL-1β, IL-8, and tumor necrosis factor (TNF)-α in culture supernatants of THP-1 cells were measured by enzyme-linked immunosorbent assay. A luciferase reporter assay was conducted to confirm the interaction of miRNA and IL-1β 3′-untranslated regions (UTRs). Combining bioinformatics and miRNA expression profiles, we found five miRNAs (hsa-miR-30c-1-3p, hsa-miR-488-3p, hsa-miR-550a-3p, hsa-miR-663a, and hsa-miR-920) that possibly target IL-1β. Then, we demonstrated that miR-488 and miR-920 were significantly decreased in the WBCs of patients with GA and that MSU crystals could inhibit expression of miR-488 and miR-920. Upregulation of miR-488 and miR-920 could suppress MSU-induced IL-1β protein expression in THP-1 cells, but no significant difference in IL-1β messenger RNA levels was observed. Moreover, we found that miR-488 and miR-920 could directly target the 3′-UTR of IL-1β. Overexpression of miR-488 and miR-920 could significantly inhibit the gene and protein expression of IL-8 and TNF-α in MSU-induced THP-1 cells. This study demonstrates the roles of miR-488 and miR-920 in regulating the production of proinflammatory cytokines in the pathogenesis of GA. These findings suggest that miR-488 and miR-920 could serve as potential therapeutic targets in the treatment of GA.

Aim: To explore the circular RNA (circRNA) profile in cumulus cells from endometriosis-associated infertility patients. Methods: The expression of circRNAs was profiled by high-throughput sequencing. Sanger sequencing was performed to identify the backsplicing site. Six candidate circRNAs and their parental genes were measured in 30 samples by quantitative reverse transcription-polymerase chainreaction (qRT-PCR). Bioinformatics analysis was performed to predict the functions. Results: A total of 55 upregulated and 41 downregulated differentially expressed circRNAs were detected. Kyoto Encyclopedia of Genes and Genomes data indicated that these target genes were mainly involved in cumulus cell growth- and differentiation-related pathways. Hsa_circ_0072391, hsa_circ_0007299 and hsa_circ_0057799 were significantly increased, and hsa_circ_001533 was significantly decreased in endometriosis-associated infertility patients. Conclusion: The differentially expressed circRNAs might be potentially involved in pathophysiology of endometriosis-associated infertility.

Purpose: This study was designed to reveal the molecular differences between granulosa cells (GCs) from patients with endometriosis and normal controls. Methods: RNA sequencing was performed on GCs from patients with EM-related infertility (n = 3) and controls (n = 3). Differentially expressed long noncoding RNAs [differentially expressed lncRNAs (DELs), |log2 FC|>4, false discovery rate (FDR) 1.4, FDR <0.05] in patients with EM-related infertility and controls were screened. Protein–protein interaction (PPI) networks of the DEGs were constructed. Then, mRNA–miRNA–lncRNA pairs based on DEGs and DELs were constructed by comprehensive bioinformatics analyses. In addition, overlapping genes identified from both the PPI and the mRNA–miRNA–lncRNA pairs were selected. Finally, a competing endogenous RNA (ceRNA) network incorporating transcription factors (TFs) was constructed. Results: A total of 25,806 lncRNAs and 19,684 mRNAs were detected, and 7 DELs and 46 DEGs were identified. Five hub genes from the PPI network were also identified. A single overlapping gene, NR4A2, from both the PPI network and mRNA–miRNA–lncRNA pairs was identified. Finally, a ceRNA network incorporating TFs, including one mRNA (NR4A2), one miRNA (hsa-miR-217), three lncRNAs (XIST, MCM3AP-AS1, and C17orf51), and five TFs (SRF, POLR2A, NRF1, MNT, and TCF7L2), was successfully constructed. Conclusions: The proposed ceRNA network and the prediction of TFs in GCs from EM-related infertility revealed differences in GCs from patients with EM. Importantly, the novel TFs, lncRNAs, miRNAs, and mRNAs involved in the ceRNA network might provide new insights into the underlying molecular mechanisms of EM-related infertility.

Objective: This study aimed to assess the effects of the Jinfeng pill on ovarian volume and endocrine function in rats with poor ovarian response and to elucidate the gene expression changes that contribute to the Jinfeng pill’s role in improving ovarian function. Methods: Thirty 8-week-old specific pathogen-free (SPF) female rats were randomly assigned to five groups: control, model, estradiol, Jinfeng pill, and Jinfeng pill + estradiol, with six rats in each group. All groups, except the control were administered Tripterygium glycoside tablets. After establishing the poor ovarian response model, the three intervention groups (estradiol, Jinfeng pill, and Jinfeng pill + estradiol) received their respective drug interventions. Hematoxylin-eosin staining was employed to assess follicle distribution, and immunohistochemistry was used to evaluate the expression of vascular endothelial growth factor and endostatin in rat ovaries. Hormone levels were measured using ELISA. Results: The uterine and total ovarian masses in the three intervention groups were higher than those in the model group; however, the differences were not statistically significant. The ovaries of the Jinfeng pill and Jinfeng pill + estradiol groups contained more follicles at various developmental stages. The three intervention groups showed significantly increased vascular endothelial growth factor expression and decreased endostatin expression compared with the model group, with the Jinfeng pill + estradiol group exhibiting the most pronounced differences. Anti-Müllerian hormone levels were slightly elevated in the Jinfeng pill group compared to the model group. However, only the Jinfeng pill + estradiol group showed a statistically significant decrease in follicle-stimulating hormone levels compared to the model group (P = 0.01). Conclusions: Jinfeng pill modulates ovarian protein expression, increases ovarian volume, and improves blood circulation. Additionally, it may elevate hormone levels and enhance ovarian response function in rats with poor ovarian function.