Main content area

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

Chen, Mei-Fen, Liou, Shorong-Shii, Kao, Shung-Te, Liu, I-Min
Food and chemical toxicology 2019 v.126 pp. 97-105
Dendrobium chrysotoxum, adenosine triphosphate, apoptosis, caspases, cell viability, cytochrome c, diabetic nephropathy, epithelial cells, glucose, glutathione, malondialdehyde, membrane potential, mitochondrial membrane, mitogen-activated protein kinase, protective effect, reactive oxygen species, signal transduction, therapeutics, toxicology, transcription factor NF-kappa B
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.