Investigation of MicroRNA-17 Expression, Tumor Necrosis Factor-α, and Interleukin-6 Levels in Lumbar Degenerative...

Background/Objectives: The aim of the study is to investigate the role of microRNA-17 (miRNA-17), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) in the pathogenesis of lumbar degenerative disc disease (LDDD). The goal is to explore how miRNA-17 regulates inflammation and apoptosis within the intervertebral discs, with a particular focus on its involvement in inflammatory pathways via NF-κB signaling. This research seeks to uncover the molecular mechanisms that contribute to LDDD and its associated chronic lower back pain and disability. Methods: A case-control study was conducted, involving 110 patients diagnosed with LDDD and 17 healthy control individuals. Serum levels of miRNA-17, TNF-α, and IL-6 were measured using quantitative real-time PCR and enzyme-linked immunosorbent assays (ELISAs). The patients were further categorized based on the severity of their condition using the Oswestry Disability Index (ODI), which classified them into five subgroups. The correlation between miRNA-17 expression, pro-inflammatory cytokines, and disease severity was analyzed statistically. Results: The results demonstrated a significant downregulation of microRNA-17 in patients with LDDD compared to healthy controls. Inflammatory markers TNF-α and IL-6 were found to be significantly elevated in the patient group. A peak in inflammation and miRNA-17 expression was observed in patients with moderate to severe disability (ODI Grade 3), while inflammation levels decreased in more advanced stages of the disease (ODI Grades 4 and 5), suggesting a possible shift in disease dynamics. Conclusions: This study demonstrates that miRNA-17 plays a regulatory role in inflammation during the progression of LDDD, particularly through the modulation of TNF-α and IL-6 levels. The findings indicate that inflammation is most pronounced in the mid-stages of LDDD, while the later stages are characterized by structural damage rather than ongoing inflammation. These insights could help guide future therapeutic strategies aimed at targeting the molecular mechanisms underlying LDDD, potentially improving patient outcomes.