Nobiletin suppresses high‐glucose–induced inflammation and ECM accumulation in human mesangial cells through STAT3/NF‐κB pathway
| Autor: | Junlei Tian, Yanru Han, Zhenxia Zhao, Kui Jia, Zhenzhou Liu, Fucheng Zhao |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
STAT3 Transcription Factor
0301 basic medicine Glomerular Mesangial Cell Anti-Inflammatory Agents Inflammation Biochemistry Antioxidants Nobiletin Extracellular matrix 03 medical and health sciences chemistry.chemical_compound Glomerular mesangial cell proliferation 0302 clinical medicine medicine Humans STAT3 Molecular Biology biology Chemistry NF-kappa B Cell Biology Flavones Extracellular Matrix Oxidative Stress Glucose 030104 developmental biology Gene Expression Regulation Sweetening Agents 030220 oncology & carcinogenesis Mesangial Cells biology.protein Cancer research Cytokine secretion Tumor necrosis factor alpha medicine.symptom |
| Zdroj: | Journal of Cellular Biochemistry. 120:3467-3473 |
| ISSN: | 1097-4644 0730-2312 |
| DOI: | 10.1002/jcb.27621 |
| Popis: | Diabetic nephropathy (DN) is a complication of chronic diabetes and the main cause of end-stage renal disease all over the world. Inflammation and extracellular matrix (ECM) accumulation play important roles in the pathogenesis of DN. Evidence suggested that nobiletin acts anti-inflammatory role and plays a critical role in diabetes; however, its role in DN remains unclear. In the current study, we promulgated the nobiletin involved in high-glucose-induced glomerular mesangial cell inflammation and ECM accumulation. Nobiletin treatment significantly abrogated high-glucose-induced glomerular mesangial cell proliferation. Nobiletin treatment markedly suppressed inflammation cytokine secretion, including interleukin (IL)-1β, IL-6, tumor necrosis factor α, and monocyte chemoattractant protein 1 in high-glucose-induced glomerular mesangial cell. Also, exposed nobiletin to high-glucose-induced glomerular mesangial cell considerably reduced ECM accumulation through inhibited ECM-associated protein type 4 collagen and fibronectin expression. Furthermore, nobiletin treatment abolished nuclear factor κB (NF-κB) pathway activation through signal transducer and activator of transcription 3 (STAT3) inhibition. Overexpression STAT3 reversed the effects of nobiletin on high-glucose-induced glomerular mesangial cell proliferation, inflammation, ECM accumulation, and NF-κB pathway activation. Hence, our results suggest that nobiletin play roles in high-glucose-induced glomerular mesangial cells through inhibiting inflammation and ECM accumulation, and the STAT3/NF-κB pathway was involved in the function of nobiletin. |
| Databáze: | OpenAIRE |
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