Osteoarthritis(OA)is a degenerative joint disease primarily characterized by articular cartilage degeneration.Autophagy is a crucial intracellular homeostatic system that plays a vital role in maintaining normal cartilage function.By regulating cell apoptosis and repairing damaged chondro-cytes,autophagy protects cartilage,and dysfunction in chondrocyte autophagy is an important patho-genic mechanism underlying cartilage degeneration in OA.MicroRNAs(miRNA)can regulate gene expression and play a key role in chondrocyte development and functional maintenance.MiRNA in-volved in the regulation of autophagy are aberrantly expressed in OA,suggesting that miRNAs may serve as potential targets and biomarkers for early prediction,diagnosis,and effective treatment of OA.This review discussed the role of autophagy in OA and the regulatory role of miRNA in OA de-velopment,with a focus on the role of miRNA-mediated regulation of chondrocyte autophagy in OA pathogenesis and its potential therapeutic value.

Spinal cord injury (SCI) is a disabling and destructive central nervous system injury that has not yet been successfully treated at this stage. Three-dimensional (3D) bioprinting has become a promising method to produce more biologically complex microstructures, which fabricate living neural constructs with anatomically accurate complex geometries and spatial distributions of neural stem cells, and this is critical in the treatment of SCI. With the development of 3D printing technology and the deepening of research, neural tissue engineering research using different printing methods, bio-inks, and cells to repair SCI has achieved certain results. Although satisfactory results have not yet been achieved, they have provided novel ideas for the clinical treatment of SCI. Considering the potential impact of 3D bioprinting technology on neural studies, this review focuses on 3D bioprinting methods widely used in SCI neural tissue engineering, and the latest technological applications of bioprinting of nerve tissues for the repair of SCI are discussed. In addition to introducing the recent progress, this work also describes the existing limitations and highlights emerging possibilities and future prospects in this field.

Syringaresinol-4---d-glucoside (SSG), a furofuran-type lignan, was found to modulate lipid and glucose metabolism through an activity screen of lipid accumulation and glucose consumption, and was therefore considered as a promising candidate for the prevention and treatment of metabolic disorder, especially in lipid and glucose metabolic homeostasis. In this study, the effects of SSG on lipogenesis and glucose consumption in HepG2 cells and C2C12 myotubes were further investigated. Treatment with SSG significantly inhibited lipid accumulation by oil red O staining and reduced the intracellular contents of total lipid, cholesterol and triglyceride in HepG2 cells. No effect was observed on cell viability in the MTT assay at concentrations of 0.1-10 μmol/L. SSG also increased glucose consumption by HepG2 cells and glucose uptake by C2C12 myotubes. Furthermore, real-time quantitative PCR revealed that the beneficial effects were associated with the down-regulation of sterol regulatory element-binding proteins-1c, -2 (), fatty acid synthase (), acetyl CoA carboxylase () and hydroxyl methylglutaryl CoA reductase (), and up-regulation of peroxisome proliferator-activated receptors alpha and gamma (and). SSG also significantly elevated transcription activity oftested by luciferase assay. These results suggest that SSG is an effective regulator of lipogenesis and glucose consumption and might be a candidate for further research in the prevention and treatment of lipid and glucose metabolic diseases.