Background/Aim: Increased oxidative stress plays a crucial role in pathogenesis of various diseases. The present study aims to investigate glutathione reductase (GR) and malondialdehyde (MDA) enzymes as markers of oxidative stress mechanisms in lumbar disc degeneration disease (LDDD). Patients and Methods: The study group consisted of 39 patients diagnosed with LDD and 37 healthy individuals in the control group. The enzyme-linked immunosorbent assay (ELISA) method was used to determine serum GR and MDA levels in the two study groups. Results: Serum GR levels were significantly lower (p=0.008), while MDA levels were significantly higher in the patient group compared to the controls (p=0.025). Conclusion: Oxidative stress mechanisms play a crucial role in disc degeneration and GR deficiency could be an eligible risk factor for LDDD.

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.

Lumbar degenerative disc disease (LDDD) is characterized by persistent inflammation and extracellular matrix degradation. Emerging as main controllers in its pathogenesis are microRNAs (miRNAs) and proinflammatory cytokines. Through the JAK/STAT signalling pathway, HSA-miR-186-5p has been linked to modulating cytokine expression, including interleukin-2 (IL-2). The aim is to find the expression levels of IL-2 and HSA-miR-186-5p in LDDDpatients and investigate their possible correlation with disease degree. 110 LDDD patients and 17 healthy controls wereincluded. ELISA measured serum IL-2 concentrations, and RT-qPCRestimated miR-186-5p levels. The Oswestry Disability Index (ODI) guidedpatients into five subgroups (G1–G5). One-way ANOVA and correlationanalysis were applied in statistical comparisons. LDDD patients had notably higher IL-2 levels than controls ( p <0.001). According to the subgroup analysis, the IL-2 concentration peaked inG2 and G3 and gradually dropped toward G5. By contrast, miR-186-5pexpression was noticeably lowered in the LDDD group ( p < 0.001), with G1and G5 having the lowest levels found. Across groups, an inverse trend in IL-2 and miR-186-5p expression was noted. Results imply a dysregulated interaction between HSA-miR-186-5p and IL-2 in LDDD. Particularly in early and moderate stages ofdisease, miR-186-5p downregulation could help to explain increased IL-2-mediated inflammation. These biomarkers could provide information ondisease activity and present targets for new treatments.

Ovarian cancer is frequently diagnosed at an advanced stage due to non-specific symptoms, contributing to high mortality. The limited diagnostic performance of current serum assays in early disease underscores the need for complementary circulating biomarkers. Circulating microRNAs and inflammation-related markers are promising candidates. Although miRNAs are implicated in cancer diagnostics, the role of miRNA-29a in ovarian cancer remains underexplored. Given that sST2 is elevated in several malignancies and is a direct target of miRNA-29a, concurrent evaluation may be informative. This pilot study compared serum miRNA-29a and sST2 levels in 23 ovarian cancer patients and 22 healthy female controls. miRNA-29a expression was quantified by real-time PCR (2^−ΔΔCt), and sST2 was measured by ELISA; diagnostic performance was assessed using ROC analysis. miRNA-29a levels were significantly reduced (p < 0.05), whereas sST2 concentrations were significantly increased (p < 0.001) in patients versus controls. ROC analysis showed modest discrimination for miRNA-29a (AUC 0.678) and higher performance for sST2 (AUC 0.825). No significant correlation was observed between the two markers. These findings suggest that circulating miRNA-29a and sST2 may have biomarker potential in ovarian cancer; larger, well-designed studies are required to confirm clinical utility.