Deoxyactein protects pancreatic β-cells against methylglyoxal-induced oxidative cell damage by the upregulation of mitochondrial biogenesis

摘要: Abstract Methylglyoxal (MG) is one of the major precursors advanced glycation end products (AGEs), which are considered to be causes diabetes and its complications. The root rhizomes black cohosh (Cimicifuga racemosa) have long been used medicinally, deoxyactein constituents. In present study, protective effects against MG-induced oxidative cell damage were investigated in insulin-producing pancreatic β-cells. We found that protected β-cells death. Pre-treatment with significantly reduced levels intracellular reactive oxygen species (ROS), interleukin-1β (IL-1β), cardiolipin peroxidation, protein adduct accumulation induced by MG. cells restored glyoxalase I activity insulin secretion MG, increased mRNA expression insulin 2 (INS2) duodenal homeobox protein-1 (PDX-1). It also endogenous antioxidant enzymes, including superoxide dismutase (SOD) glutathione peroxidase (GPX). Furthermore, treatment sirtuin 1 (SIRT1) peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α). These findings indicate may exert beneficial on via upregulation mitochondrial biogenesis. Taken together, these results suggest for prevention β-cell damage.