Molecular Biology Reports最新文献

Background: Bioactive compounds are recognized for their ability to modulate immune cell activity and reduce inflammation. Polyphenols derived from Aronia leaves offer multiple biological activities; however, their role in regulating inflammatory responses remains poorly understood. This study aimed to evaluate the anti-inflammatory activity of Aronia melanocarpa leaf phenolic extract (APE) in LPS-stimulated RAW264.7 cells.

Methods and results: At concentrations up to 50 µg/mL, APE exerted no cytotoxic effects in MTT assays performed with and without 1 µg/mL LPS-stimulated macrophages. APE significantly inhibited nitric oxide production in LPS-stimulated cells, as determined by the Griess method. Furthermore, treatment with APE (10, 25, 50 µg/mL) effectively decreased mRNA and protein expression of pro-inflammatory mediators, including IL-1β, COX-2 and iNOS, as analyzed by qPCR and Western blot, respectively. Additionally, Western blot analysis showed that APE modulated the NF-κB signaling pathway by downregulating the phosphorylation of NF-κB p65 and IκB-α, thereby suppressing NF-κB activation in LPS-stimulated RAW264.7 cells.

Conclusions: The findings suggest that polyphenols in Aronia leaves exert potent anti-inflammatory effects by inhibiting the NF-κB signaling pathway and suppressing pro-inflammatory mediators. Therefore, Aronia leaf extract may serve as a promising candidate for the development of therapeutic agents that support the treatment of inflammation-related diseases.

Background: Diabetic nephropathy (DN) is a major complication of type 1 diabetes (T1D). Current diagnostic parameters, such as albuminuria and estimated glomerular filtration rate (eGFR), often detect the disease at advanced stages, promoting the identification of additional inflammatory markers. This study investigated the potential roles of pro-inflammatory interleukin-26 (IL-26), anti-inflammatory interleukin-35 (IL-35), and Signal Transducer and Activator of Transcription 1 (stat1) gene expression as potential biomarkers of DN in T1D.

Objective: To evaluate serum levels of IL-26 and IL-35 and the gene expression of stat1 in T1D patients with and without renal dysfunction to assess their involvement in DN.

Materials and methods: This case-control study included 80 T1D patients (subgrouped to nephropathy status) and 60 healthy controls. Serum cytokine levels were measured using enzyme-linked immunosorbent assay (ELISA), and stat1 expression in the blood was assessed using quantitative real-time PCR (qPCR). Statistical analyses included ANOVA, correlation tests, and receiver operating characteristic (ROC) curve analysis.

Results: IL-26 levels were not significantly elevated in hemodialysis T1D patients. IL-35 levels were significantly higher in T1D patients with nephropathy and in those on hemodialysis. A significant positive correlation was observed between IL-26 and IL-35 levels (r = 0.561, p = 0.0002). stat1 gene expression was significantly elevated in all T1D subgroups compared to controls, with the highest level observed in the hemodialysis group. ROC analysis indicated that stat1 had a discriminative ability for T1D, whereas IL-35 showed an acceptable diagnostic value for end-stage renal disease.

Conclusion: This study showed that stat1 expression and IL-35 levels were linked with renal impairment in the T1D context, with stat1 expression elevated across T1D subgroups, and IL-35 expression was more accentuated in advanced renal dysfunction. Despite its limited discriminative value, IL-26 correlates with IL-35, suggesting simultaneous regulation within the inflammatory microenvironment.