The inflammatory response has an important role in the pathophysiology of diabetic nephropathy that is contributed to by inflammatory mediators such as interleukin-1 (IL-1), IL-6, IL-18, tumor necrosis factor-α, and macrophage chemotactic protein-1; however, the role of IL-18 seems to be more specific than other cytokines in the inflammatory process.
Compared to the NO-CKD group, the NA-DKD group was older with lower hemoglobin (HB) levels and higher systolic blood pressure (SBP), plasma TNF-<i>α</i>, IL-6, and 8-OHdG levels.
In this study, our aim was to investigate the role of fetuin-A in relation with pro-inflammatory cytokines (IL-6, IL-18), adipokines (adiponectin, leptin), chemokine (MCP-1), and adhesion molecules (ICAM-1, VCAM-1) in control and DKD subjects.
It is shown that the TNF signaling pathway plays a role through the process of DN progression and adipocytokine signaling pathway is uniquely enriched in ESRD.Molecules, such as TNF, IL6, SOD2, etc. are very important for DN progression, among which, it seems that "AGER" plays a pivotal role in the mechanism.
And then, blood glucose, urine protein, renal index, renal microstructural (HE/PAS staining), inflammatory factors (IL-<i>β</i>, TNF-<i>α</i>, IL-6), and protein/mRNA expression related to the function of podocyte (CD2AP and Podocin) in DN rats were investigated after the oral administration of EZF.
Inflammatory cytokines such as interleukin 1 (IL-1), IL-6, IL-18 and tumor necrosis factor-α (TNFα) have been linked to the development and progression of DN.
The presence of DN involved a lower leukocyte rolling velocity and an increased rolling flux and adhesion. miR-31 levels were positively correlated with leukocyte rolling velocity and negatively associated to leukocyte adhesion, TNFα, IL-6 and ICAM-1 levels.
The results showed that mulberry leaf powder contains tricetin, gallic acid, chlorogenic acid, and other drug components that can regulate tumor necrosis factor (TNF), peroxisome proliferator-activated receptor gamma (PPARG), glycogen synthase kinase-3 beta (GSK3B), insulin receptor substrate 1 (IRS1), interleukin 6 (IL-6) and other proteins, which are related to the insulin and inflammatory signaling pathways, glucose metabolism and other related pathways, chronic inflammatory diseases, obesity, diabetic nephropathy, non-insulin-dependent diabetes mellitus and other diseases.
The suppressive effects of PTNE on creatinine, blood urea nitrogen, interleukin (IL)‑2, IL‑6 and nuclear factor‑κB levels indicated its ability to provide protection against diabetic nephropathy.
To address this, the DN model was established, and oxidative stress indexes, including malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH‑Px), and inflammatory cytokines, includinginterleukin‑6 (IL‑6), tumor necrosis factor‑alpha (TNF‑α) and transforming growth factor‑beta (TGF‑β), were examined by ELISA.
The biomarker profiles associated with mortality differed significantly by CKD etiology as follows: DKD was associated with CysC (HR 1.3, 95% CI 1.0-1.6), ADMA (HR 1.3, 95% CI 1.1-1.6), and NT-proBNP (HR 1.7, 95% CI 1.4-2.1), GN was associated with FGF23 (HR 1.8, 95% CI 1.1-2.8), TnI (HR 3.6, 95% CI 1.3-9.5), and transforming growth factor-beta (HR 0.6, 95% CI 0.4-0.9) and PCK/TIN was associated with ADMA (HR 1.5, 95% CI 1.3-1.8) and IL-6 (HR 2.1, 95% CI 1.5-3.1).
Pro-inflammatory cytokines, such as interleukin-6 (IL-6), have been considered as key factors in type 1 diabetes mellitus (T1DM) and diabetic nephropathy, thus, our aim was to investigate the association of IL6-174G>C (rs1800795) and -634C>G (rs1800796) polymorphisms with T1DM susceptibility and diabetic nephropathy.
Compared to the normal control, LPS and IL-15 down-regulate monocytic VDR expression in T2DM patients and DN uremic patients, whilst with cytoskeletal rearrangement, they up-regulate p-STAT5 expression as well as IL-6 and MCP-1 activity.