BackgroundArticular cartilage diseases are considered a major health problem, and tissue engineering using human mesenchymal stem cells (MSCs) have been shown as a promising solution for cartilage tissue repair. Hesperidin is a flavonoid extract from citrus fruits with anti-inflammatory properties. We aimed to investigate the effect of hesperidin on MSCs for cartilage tissue repair. MSCs were treated by hesperidin, and colony formation and proliferation assays were performed to evaluate self-renewal ability of MSCs. Alcian blue staining and Sox9 expression were measured to evaluate chondrogenesis of MSCs. Secretion of pro-inflammatory cytokines IFN-γ, IL-2, IL-4 and IL-10, and expression of nuclear factor kappa B (NF-κB) subunit p65 were also assessed.ResultsHesperidin improved self-renewal ability and chondrogenesis of MSCs, inhibited secretion of pro-inflammatory cytokines IFN-γ, IL-2, IL-4 and IL-10, and suppressed the expression of p65. Overexpression of p65 was able to reverse the hesperidin inhibited secretions of pro-inflammatory cytokines, and abolish the enhancing effect of hesperidin on chondrogenesis of MSCs.ConclusionHesperidin could serve as a therapeutic agent to effectively enhance chondrogenesis of human MSCs by inhibiting inflammation to facilitate cartilage tissue repair.Electronic supplementary materialThe online version of this article (10.1186/s12950-018-0190-y) contains supplementary material, which is available to authorized users.

This study was aimed to investigate the relationship between miR-221 expression and prognosis in patients with osteosarcoma.miR-221 expression in 69 osteosarcoma specimens and corresponding noncancer tissues were characterized by quantitative reverse transcription polymerase chain reaction. The associations of miR-221 expression with clinicopathologic factors and prognosis in patients with osteosarcoma were statistically analyzed.miR-221 expression in patients with osteosarcoma was significantly higher than in the corresponding noncancer tissues (P < .01). miR-221 overexpression was significantly associated with tumor stage, metastatic status, and response to chemotherapy pretreatment. Cox regression analysis revealed that miR-221expression, metastasis, and response to chemotherapy were independent prognostic indicators for osteosarcoma.miR-221 upregulation may predict clinical outcomes in patients with osteosarcoma.

Background: Osteoarthritis (OA) is a major factor causing pain and disability. Studies performed to date have suggested that synovitis is possibly a critical OA-related pathological change. Ferroptosis represents a novel type of lipid peroxidation-induced iron-dependent cell death. However, its effect on OA remains largely unclear.Objective: This work focused on identifying and validating the possible ferroptosis-related genes (FRGs) involved in synovitis of OA through bioinformatics analysis.Materials and Methods: The microarray dataset GSE55235 was downloaded in the database Gene Expression Omnibus (GEO). By the Venn diagram and GEO2R, differentially expressed genes (DEGs) and ferroptosis DEGs (FDEGs) were detected. DEGs were screened by GO and KEGG enrichment analysis, as well as protein-protein interaction (PPI) analysis. Besides, the software Cytoscape and database STRING were utilized to construct hub gene networks. Moreover, this study used the database NetworkAnalyst to predict the target miRNAs of the hub genes. Finally, the hub genes were confirmed by analysis of the receiver operating characteristic (ROC) curve on the GSE12021 and GSE1919 databases. Considering the relationship between ferroptosis and immunity, this study applied CIBERSORTx to analyze the immune infiltration in OA in addition.Results: This work discovered seven genes, including ATF3, IL6, CDKN1A, IL1B, EGR1, JUN, and CD44, as the hub FDEGs. The ROC analysis demonstrated that almost all hub genes had good diagnostic properties in GSE12021 and GSE 1919.Conclusion: This study discovered seven FDEGs to be the possible diagnostic biomarkers and therapeutic targets of synovitis during OA, which sheds more light on the pathogenesis of OA at the transcriptome level.

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