cellobial and Inflammation

The cellular and molecular mechanisms through which cisplatin induces nephrotoxicity have been investigated extensively. However, the role of long non-coding RNAs (lncRNAs) in cisplatin-induced nephrotoxicity is not well known. We explored the functions and underlying mechanisms of a novel lncRNA XLOC_032768 in cisplatin-induced nephrotoxicity. Cisplatin treatment resulted in the apoptosis of the renal tubular epithelial cells and inflammatory response in a mouse model and human renal proximal tubular epithelial cells (HK-2). The differentially expressed genes (DEGs) of the transcriptome data were determined, and the results showed that lncRNA XLOC_032768 expression was significantly repressed by cisplatin treatment. This result was validated by an RT-qPCR experiment on in vivo and in vitro models. The overexpression of XLOC_032768 significantly inhibited the cisplatin-induced apoptosis and inflammatory response in HK-2 cells and mouse exposed to cisplatin. RNA sequencing analysis further confirmed that XLOC_032768 could regulate tumor necrosis factor (TNF)-α in the cisplatin-induced apoptosis of HK-2 cells in trans-manner. TNF-α inhibition also ameliorated cisplatin-induced apoptosis of renal tubular epithelial cells and renal structural damage. As such, XLOC_032768 suppressed cisplatin-induced apoptosis and inflammatory response of renal tubular epithelial cells through TNF-α. LncRNA XLOC_032768 is a potential novel agent to reduce cisplatin-induced nephrotoxicity.

Topics: Acute Kidney Injury; Animals; Apoptosis; Cellobiose; Cisplatin; Drug-Related Side Effects and Adverse Reactions; Epithelial Cells; Humans; Inflammation; Kidney Tubules; Male; Mice; Mice, Inbred C57BL; RNA, Long Noncoding; Tumor Necrosis Factor-alpha

Inflammation is a hallmark of many metabolic diseases. We previously showed that ferrocene-appended 1

Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Cell Survival; Cellobiose; Crystallography, X-Ray; Cyclooxygenase 2; Free Radicals; Group IV Phospholipases A2; Humans; Inflammation; Kidney Diseases; Lipopolysaccharides; Matrix Metalloproteinase 9; Mesangial Cells; Mitochondria; Molecular Docking Simulation; Nitric Oxide; Nitric Oxide Synthase Type II; Rats; Triazoles