Purpose: Steroid-induced osteonecrosis of the femoral head (SONFH) is a refractory orthopaedic hip joint disease that occurs in young- and middle-aged people. Previous experimental studies have shown that autophagy might be involved in the pathological process of SONFH, but the pathogenesis of autophagy in SONFH remains unclear. We aimed to identify and validate the key potential autophagy-related genes involved in SONFH to further illustrate the mechanism of autophagy in SONFH through bioinformatics analysis. Methods: The GSE123568 mRNA expression profile dataset, including 10 non-SONFH (following steroid administration) samples and 30 SONFH samples, was downloaded from the Gene Expression Omnibus (GEO) database. Autophagy-related genes were obtained from the Human Autophagy Database (HADb). The autophagy-related genes involved in SONFH were screened by intersecting the GSE123568 dataset with the set of autophagy genes. The differentially expressed autophagy-related genes involved in SONFH were identified with R software. In addition, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of the differentially expressed autophagy-related genes involved in SONFH were conducted by using R software. Then, the correlations between the expression levels of the differentially expressed autophagy-related genes involved in SONFH were confirmed with R software. Moreover, the protein–protein interaction (PPI) network was analysed by using the Search Tool for the Retrieval of Interacting Genes (STRING), significant gene cluster modules were identified with the MCODE Cytoscape plugin, and hub genes among the differentially expressed autophagy-related genes involved in SONFH were screened by using the CytoHubba Cytoscape plugin. Finally, the expression levels of the hub genes of the differentially expressed autophagy-related genes involved in SONFH were validated in hip articular cartilage specimens from necrotic femur heads (NFHs) by using the GSE74089 dataset and further verification by qRT-PCR. Results: A total of 34 differentially expressed autophagy-related genes were identified between the peripheral blood samples of SONFH patients and non-SONFH patients based on the defined criteria, including 25 upregulated genes and 9 downregulated genes. The GO and KEGG pathway enrichment analyses revealed that these 34 differentially expressed autophagy-related genes involved in SONFH were particularly enriched in death domain receptors, the FOXO signalling pathway and apoptosis. Correlation analysis revealed significant correlations among the 34 differentially expressed autophagy-related genes involved in SONFH. The PPI results demonstrated that the 34 differentially expressed autophagy-related genes interacted with each other. Ten hub genes were identified by using the MCC algorithms of CytoHubba. The GSE74089 dataset showed that TNFSF10, PTEN and CFLAR were significantly upregulated while BCL2L1 was significantly downregulated in the hip cartilage specimens, which was consistent with the GSE123568 dataset. TNFSF10, PTEN and BCL2L1 were detected with consistent expression by qRT-PCR. Conclusions: Thirty-four potential autophagy-related genes involved in SONFH were identified via bioinformatics analysis. TNFSF10, PTEN and BCL2L1 might serve as potential drug targets and biomarkers because they regulate autophagy. These results expand the autophagy-related understanding of SONFH and might be useful in the diagnosis and prognosis of SONFH.

Background: Knee osteoarthritis (KOA) is a prevalent degenerative joint disorder causing significant pain and functional impairment. Intra-articular injections (IAI) under ultrasound (US) guidance have emerged as a key treatment for early-to-mid stage KOA due to enhanced precision and localized therapeutic effects. However, the relative efficacy of various injectable agents remains unclear. Methods: A Bayesian network meta-analysis (BNMA) was conducted following PRISMA guidelines using the following databases: ClinicalTrials.gov , EMBASE, PubMed, Web of Science, Cochrane Library, and the WHO International Clinical Trials Registry Platform (WHO ICTRP), we searched incorporating 14 randomized controlled trials (RCTs) involving 934 patients. Interventions included US-guided injections of platelet-rich plasma (PRP), hyaluronic acid (HA), corticosteroids (CS), ozone (O3), dexamethasone (DX), autologous adipose tissue (AAT), and placebo (PL). Primary outcomes were Visual Analog Scale (VAS) and WOMAC subscale scores. Model consistency, transitivity, and robustness were rigorously assessed. Results: The analysis demonstrated that all active interventions provided significant symptom relief. PRP consistently ranked highest across multiple outcomes, with surface under the cumulative ranking curve (SUCRA) values of 85.86% for total WOMAC score, 78.55% for pain, 93.24% for stiffness, and 90.9% for function. HA showed significant superiority over ozone in pain reduction (SMD: −1.48, 95% CI: −2.71 to −0.24). Model consistency was confirmed ( p > 0.05 for all node-splitting tests), and sensitivity analyses supported result stability. No significant publication bias was detected. Conclusion: IAI under US-guided has shown good therapeutic effect in the treatment of KOA in the early and middle stages, and PRP has been proved to have the highest therapeutic possibility, followed by HA and CS. These findings support the use of US-guided biologic interventions as part of a comprehensive KOA management strategy, though standardization of protocols and long-term outcomes require further investigation.

Objective: This study aims to evaluate the antioxidant, anti-aging, and mitochondrial protective effects of JadeAging, a Chinese medicine-based longevity formulation, using the model organism Caenorhabditis elegans . Methods: We used C. elegans to assess the impact of JadeAging and its individual components (rehmannia, poria, and ginseng) on various health metrics. RNA sequencing (RNA-seq) was performed to identify differentially expressed genes and their effects on biological pathways. Lifespan and healthspan assays were performed to evaluate cell vitality, whereas mitochondrial health was assessed using mitochondrial fragmentation analysis. Antioxidant capacity was determined by measuring protection against reactive oxygen species Results: Treatment with JadeAging did not significantly extend lifespan but showed improvements in healthspan, with treated animals exhibiting more vigorous movement over their lifespan. JadeAging and its components demonstrated significant antioxidant capacity, protecting C. elegans from the deleterious effects of paraquat-induced oxidative stress. Furthermore, JadeAging treatment significantly reduced mitochondrial fragmentation, indicating enhanced mitochondrial health. RNA-Seq data revealed downregulation of daf-2 and rsks-1 and upregulation of cpr-1, suggesting the activation of the Target of Rapamycin pathway and promotion of autophagy. Conclusion: JadeAging exerts protective effects against oxidative stress and age-related mitochondrial decline, likely by modulating key longevity pathways. These findings support the positive effects of JadeAging and its components on health.