Erianin protects against high glucose-induced oxidative injury in renal tubular epithelial cells.

Abstract Erianin is the major bibenzyl compound found in Dendrobium chrysotoxum Lindl. The current study was designed to investigate the protective effects of erianin on high glucose-induced injury in cultured renal tubular epithelial cells (NRK-52E cells) and determine the possible mechanisms for its effects. NRK-52E cells were pretreated with erianin (5, 10, 25 or 50 nmol/L) for 1 h followed by further exposure to high glucose (30 mmol/L, HG) for 48 h. Erianin concentration dependently enhanced cell viability followed by HG treatment in NRK-52E cells. HG induced reactive oxygen species (ROS) generation, malondialdehyde production, and glutathione deficiency were recovered in NRK-52E cells pretreated with erianin. HG triggered cell apoptosis via the loss of mitochondrial membrane potential, depletion of adenosine triphosphate, upregulation of caspases 9 and 3, enhancement of cytochrome c release, and subsequent interruption of the Bax/Bcl-2 balance. These detrimental effects were ameliorated by erianin. HG also induced activation of p53, JNK, p38 mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) in NRK-52E cells, which were blocked by erianin. The results suggest that treatment NRK-52E cells with erianin halts HG-induced renal dysfunction through the suppression of the ROS/MAPK/NF-κB signaling pathways. Our findings provide novel therapeutic targets for diabetic nephropathy. Highlights • High glucose caused oxidative stress and cellular damage in NRK-52E cells. • Erianin ameliorated high glucose-induced cytotoxicity in NRK-52E cells. • Erianin prevented NRK-52E cells from high glucose-induced mitochondrial dysfunction. • Erianin suppressed ROS/MAPK/NF-κB signaling in NRK - 52E cells exposed to a high glucose. [ABSTRACT FROM AUTHOR]