Inflammatory cytokines have been implicated as crucial contributors to the onset and progression of non-alcoholic fatty liver disease (NAFLD). The exact mechanisms by which interleukins (ILs) contribute to NAFLD may vary, and ongoing research is aimed at understanding the specific roles of different ILs in the pathogenesis of this condition. In addition, variations in environmental factors and genetics in each individual can influence the onset and/or progression of NAFLD. The lack of clinical studies related to the potential therapeutic properties of IL-1 inhibitors currently does not allow us to conclude their validity as a therapeutic option, although preclinical studies show promising results. Further studies are needed to elucidate their beneficial properties in NAFLD treatment.

Purpose: Symptoms and disorders related to menopause and its associated estrogen deficiency have become a considerable health concern worldwide. Ovarian hormone depletion/estrogen deficiency can be usefully studied using animal models after removal of the ovaries [ovariectomy (Ovx)]. This study assessed renal changes after Ovx-induced estrogen deficiency in a rat model. Methods: Rats were randomly allotted into one control group (group I, healthy) and three study groups (group II, Ovx group; group III, Ovx +17β-estradiol group; and group IV, Ovx + bortezomib group). Results: In the Ovx group (group II), thickening of glomerular capillary walls, narrowing of Bowman’s capsular space, glomerular hypertrophy, atrophic tubules, and loss of the basal membranes of the tubules were observed. Mesangial cell proliferation was observed, particularly in the glomerulus. Immunohistochemical (IHC) staining studies in this group showed dense staining in the mesangial cells, tubular cell Nf-KB/p65, and caspase-3. Groups III and IV (Ovx +17β-estradiol and Ovx + bortezomib) showed decreased NF-kB/p65 and caspase-3 expression compared with the Ovx group (p < 0.05). Conclusion: In renal failure related to estrogen deficiency caused by Ovx, 17β-estradiol and bortezomib have a protective effect on renal tissue.

Six million cancer patients worldwide receive radiotherapy, either alone or in combination with other cancer treatments annually. The purpose of this study was to investigate, at the structural and molecular levels, the protective effect of N-acetylcysteine (NAC), a powerful antioxidant, against radiotherapy-induced damage on the intestinal system. Three study groups were constituted: control (group 1: no radiotherapy), radiotherapy (RT; group 2), and RT + NAC (group 3). The NAC group received 300 mg/kg NAC orally for five days before irradiation. At the end of the 5th day, 6 Gy was irradiated once, and 300 mg/kg NAC was administered orally for two days following irradiation. NAC drug administration was maintained for a total of seven days. At the end of the study, the rats were euthanized by the administration of anesthetic agents and sacrificed. The malondialdehyde (MDA) levels and caspase-3 expression increased and glutathione (GSH) levels decreased in RT rats compared to the control group ( p < 0.05). NAC reduced MDA levels, and caspase-3 expression, and increased GSH levels in the small intestine caused by RT ( p < 0.05). Therefore, NAC may be useful in the prevention of gastrointestinal syndrome in patients undergoing radiotherapy in the treatment of malignancy. Impact statement: Some six million cancer patients currently receive radiotherapy. Radiotherapy eliminates cancer cells by accelerating their death. However, radiotherapy is not selective, and it therefore harms healthy tissues around cancerous tissue. The latest studies have shown that the irradiation of biological materials causes a rapid increase in reactive oxygen species (ROS) in the tissue as a result of exposure of the target molecule to direct and indirect ionization. N-acetylcysteine (NAC) is an antioxidant that permits the elimination of free oxygen radicals and that contributes to glutathione synthesis. Our study, therefore, examined the effects of radiation resulting from radiotherapy on the small intestine at the molecular level, and prospectively considered the potential protective characteristics of NAC against gastrointestinal syndrome resulting from radiotherapy.

Background: Despite distinct etiologies, type 1 diabetes (T1D) and type 2 diabetes (T2D) share chronic inflammation as a core feature. Interleukins, key immune mediators, play important yet still not fully understood roles in the development and complications of both conditions. Objective: This narrative review aims to provide a comprehensive and critical synthesis of current evidence on the role of key interleukins in T1D and T2D, highlighting their immunological functions, genetic associations, clinical correlations, and translational potential. Methods: A targeted literature search was conducted in PubMed, Google Scholar, and ScienceDirect up to January 2025, focusing on English-language clinical and experimental studies involving interleukins and their relevance to T1D and T2D. Reference lists were manually screened for additional sources. Interleukins (ILs) were reviewed individually to assess their immunobiology, disease specificity, and biomarker or therapeutic value. Findings: Pro-inflammatory cytokines such as IL-1β, IL-6, and IL-17 contribute to islet inflammation, insulin resistance, and microvascular damage in both T1D and T2D. Anti-inflammatory mediators including IL-4, IL-10, and IL-13 exhibit protective effects but vary in expression across disease stages. Less-characterized interleukins such as IL-3, IL-5, IL-9, and IL-27 demonstrate dual or context-dependent roles, particularly in shaping immune tolerance and tissue-specific complications such as nephropathy and neuropathy. Polymorphisms in IL-10 and IL-6 genes further suggest genetic contributions to interleukin dysregulation and metabolic dysfunction. Despite promising insights, translational gaps persist due to overreliance on preclinical models and limited longitudinal clinical data. Conclusions: Interleukins represent a mechanistic bridge linking immune dysregulation to metabolic derangements in both T1D and T2D. While their diagnostic and therapeutic potential is increasingly recognized, future research must address current limitations through isoform-specific targeting, context-aware interventions, and validation in large-scale, human cohorts. A unified interleukin-based framework may ultimately advance personalized strategies for diabetes prevention and treatment.

Endocan, or endothelial cell-specific molecule-1 (ESM-1), is a potential inflammatory marker implicated in endothelial dysfunction. The purpose of this study was to determine the correlation between serum endocan levels and the presence and severity of endothelial dysfunction, and the relationships with serum intracellular adhesion molecule-1 (ICAM-1), adiponectin (a marker of inflammation), high sensitivity C-reactive protein (hsCRP) levels, and carotid intima-media thickness (cIMT) in obese subjects. Serum endocan, ICAM-1, adiponectin, hsCRP levels, and cIMT were evaluated in 76 obese women (BMI > 30 kg/m ² ) and 53 controls (BMI < 25 kg/m ² ). ICAM-1 ( P = .01), hs-CRP (p < 0.001), and cIMT ( p < .001) were significantly higher, while adiponectin ( P = .006) was significantly lower, in obese women compared with the controls. Serum endocan levels were similar between the obese (470.5 ± 171.3 pg/mL) and controls (471.9 ± 146.3 pg/mL) ( P = .732). There was no correlation between serum endocan values and the endothelial dysfunction markers, hsCRP (r = −.021), ICAM-1 (r = −.054), adiponectin (r = .113), or cIMT (r = −.060) in obesity. Endocan is not a suitable marker of endothelial dysfunction in the context of obesity. More research is required to evaluate the role of endocan in the regulation of inflammatory processes in obesity.