Diabetes mellitus is a chronic inflammatory disease characterized by high blood glucose levels due to the absence of secretion of insulin or its inefficient use in the body. In this study, we investigated how resveratrol administration affects the renal functions and pro-inflammatory signaling pathway components in streptozotocin-induced diabetes in male Wistar rats. Rats were randomly divided into four groups: (1) control/vehicle; (2) control/20 mg/kg resveratrol; (3) diabetic/vehicle; and (4) diabetic/20 mg/kg resveratrol. In addition to renal glucose, lipid, angiopoietin-1 (ANG-1), asymmetric dimethylarginine (ADMA), erythropoietin (EPO), malondialdehyde (MDA) and neutrophil gelatinase-associated lipocalin (NGAL) content, the gene expressions of pro-inflammatory markers, including inducible nitric oxide synthase (iNOS), nuclear factor kappa B (NF-κB), nuclear factor (erythroid-derived 2) like-2 (Nrf2), and the protein contents of interleukins-1β,6,8 (IL-1β,6,8) and tumor necrosis factor-α (TNF-α) were analyzed using qRT-PCR and ELISA, respectively. The rats in the diabetes group demonstrated significantly lower terminal body weight and renal ANG-1, but significantly higher renal glucose, cholesterol, triglyceride, ADMA and MDA concentrations. Diabetes triggered inflammation in kidney tissues, reflected as an increase in NGAL level. The renal inflammation observed in the diabetes group was associated with significant upregulation of components of the pro-inflammatory pathway, iNOS, NF-κB, Nrf2, IL-1β, IL-6, IL-8 and TNF-α. To some extent, resveratrol administration reversed the diabetes-induced changes in renal tissues, suggesting that resveratrol partially protected from diabetes-induced renal failure due to its restorative activities in tissue inflammation.Abbreviations ADMA − asymmetric dimethylarginine; ANG-1 − angiopoietin-1; Diab -diabetic; EPO − erythropoietin; GAPDH − glyceraldehyde 3-phosphate dehydrogenase; HRP − horseradish peroxidase; iNOS −inducible nitric oxide synthase; 6,6,8; MDA -malondialdehyde; NGAL − neutrophil gelatinase-associated lipocalin; NF-κB − nuclear factor kappa B; NO − nitric oxide; Nrf2 − nuclear factor (erythroid-derived 2) like-2; qRT-PCR − quantitative real-time PCR; Res -resveratrol; STZ -streptozotocin; TNF-α − tumor necrosis factor-α Author's contributions: HBK, MBP and SK did the practical research work. GP and GS helped during experimental work and in writing the manuscript. MBP was responsible for the drafting of the manuscript, GS made study conception and design as well as critical revisions to the manuscript.
This study aims to assess how mean corpuscular volume (MCV), red cell distribution width (RDW), and thiol-disulphide homeostasis are altered in psoriasis patients. This is a cross-sectional review of 76 healthy volunteers and 87 psoriasis patients who were consecutively admitted to the department of dermatology. Psoriasis patients and healthy controls were statistically similar with respect to age, sex, body mass index, blood pressures, and disease duration (p > 0.05 for all). When compared to healthy controls, psoriasis patients had significantly higher MCV, RDW, C-reactive protein (CRP), disulphide, disulphide/native thiol, and disulphide/total thiol (p < 0.001 for all). However, psoriasis patients had significantly lower native thiol and native thiol/total thiol (p = 0.009 and p < 0.001, respectively). When compared to healthy controls, the patients with Psoriasis Area Severity Index (PASI) ≤ 10 and patients with PASI > 10 had significantly higher MCV, disulphide, disulphide/native thiol, and disulphide/total thiol (p < 0.001 for all). The patients with PASI ≤ 10 and patients with PASI > 10 had significantly lower native thiol/native thiol than healthy controls (p < 0.001 for all). The psoriasis patients with PASI > 10 had significantly higher RDW and CRP than healthy controls and patients with PASI ≤ 10 (p < 0.001 for all). Disulphide, disulphide/native thiol, disulphide/total thiol, and native thiol/total thiol correlate significantly with both PASI scores and disease duration. Thiol-disulphide homeostasis is enhanced in psoriasis patients. Ongoing inflammation and increased oxidative stress in psoriasis patients also trigger the formation of prooxidants which are neutralized by antioxidants such as thiols. That is why plasma thiol levels are decreased in psoriasis patients.
Background Rosacea is a chronic inflammatory cutaneous disease that can be associated with cardiometabolic disorders. Oxidative stress is included in the pathogenesis of rosacea, and thiol‐disulfide homeostasis (TDH) acts as antioxidants. Objective To evaluate the TDH and metabolic parameters in patients with rosacea. Material and Methods A total of 42 rosacea patients and 50 controls participated in this prospective study. Demographic data, clinical entities, anthropometric measurements, and laboratory findings were recorded. Additionally, TDH was measured by an automated spectrophotometric method. Results Rosacea patients had greater body mass index values (27.9 ± 5.2 kg/m² vs. 23 ± 1.4 kg/m², p < 0.001), waist‐hip ratios (0.87 ± 0.1 vs. 0.77 ± 0.8, p < 0.001), and insulin resistance (3.0 ± 2.0 vs. 1.3 ± 0.5, p < 0.001) compared with controls. Disulfide levels, the disulfide/native thiol ratio (DNTR), and the disulfide/total thiol ratio (DTTR) were increased (p < 0.05) in rosacea patients. Native thiol and total thiol levels and the native/total thiol ratio (NTTR) were decreased in rosacea patients (p < 0.05). Different rosacea subtypes had no effect on oxidative stress markers. The duration of illness and insulin resistance values significantly correlated with DNTR and DTTR in the rosacea group (p < 0.05). Conclusion Rosacea has a metabolic milieu with increased oxidative stress and insulin resistance.
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