Diphenyl Diselenide Alleviates Tert-Butyl Hydrogen Peroxide-Induced Oxidative Stress and Lipopolysaccharide-Induced Inflammation in Rat Glomerular Mesangial Cells
| Autor: | Xing Wang, Yi Huan, Shuainan Liu, Caina Li, Hui Cao, Lei Lei, Quan Liu, Wenming Ji, Sujuan Sun, Kaixun Huang, Jun Zhou, Zhufang Shen |
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| Rok vydání: | 2022 |
| Předmět: |
Lipopolysaccharides
NF-E2-Related Factor 2 Interleukin-1beta Anti-Inflammatory Agents diphenyl diselenide selenium diabetic nephropathy oxidative stress inflammation Catalysis Inorganic Chemistry Selenium tert-Butylhydroperoxide Organoselenium Compounds Benzene Derivatives Animals Hypoglycemic Agents Diabetic Nephropathies RNA Messenger Physical and Theoretical Chemistry Molecular Biology Spectroscopy Inflammation Kelch-Like ECH-Associated Protein 1 Superoxide Dismutase Tumor Necrosis Factor-alpha Organic Chemistry General Medicine Hydrogen Peroxide Computer Science Applications Rats Oxidative Stress Mesangial Cells Reactive Oxygen Species |
| Zdroj: | International Journal of Molecular Sciences; Volume 23; Issue 19; Pages: 11215 |
| ISSN: | 1422-0067 |
| Popis: | Hyperglycemia, oxidative stress, and inflammation play key roles in the onset and development of diabetic complications such as diabetic nephropathy (DN). Diphenyl diselenide (DPDS) is a stable and simple organic selenium compound with anti-hyperglycemic, anti-inflammatory, and anti-oxidative activities. Nevertheless, in vitro, the role and molecular mechanism of DPDS on DN remains unknown. Therefore, we investigated the effects of DPDS on tert-butyl hydrogen peroxide (t-BHP)-induced oxidative stress and lipopolysaccharide (LPS)-induced inflammation in rat glomerular mesangial (HBZY-1) cells and explored the underlying mechanisms. DPDS attenuated t-BHP-induced cytotoxicity, concurrent with decreased intracellular ROS and MDA contents and increased SOD activity and GSH content. Moreover, DPDS augmented the protein and mRNA expression of Nrf2, HO-1, NQO1, and GCLC in t-BHP-stimulated HBZY-1 cells. In addition, DPDS suppressed LPS-induced elevations of intracellular content and mRNA expression of interleukin (IL)-6, IL-1β and TNF-α. Furthermore, LPS-induced NFκB activation and high phosphorylation of JNK and ERK1/2 were markedly suppressed by DPDS in HBZY-1 cells. In summary, these data demonstrated that DPDS improves t-BHP-induced oxidative stress by activating the Nrf2/Keap1 pathway, and also improves LPS-induced inflammation via inhibition of the NFκB/MAPK pathways in HBZY-1 cells, suggesting that DPDS has the potential to be developed as a candidate for the prevention and treatment of DN. |
| Databáze: | OpenAIRE |
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