title: Actein protects against methylglyoxal-induced oxidative damage in osteoblastic MC3T3-E1 cells.
abstract: BACKGROUND
  Methylglyoxal (MG) is an endogenous product of glucose metabolism known to be toxic to cells and to be present in elevated concentrations under certain pathophysiological conditions. In the present study the effect of actein isolated from black cohosh on MG-induced cytotoxicity was investigated in MC3T3-E1 osteoblastic cells.
  
  
  RESULTS
  Treatment of MC3T3-E1 osteoblastic cells with actein prevented MG-induced cell death and the production of intracellular reactive oxygen species (ROS), mitochondrial superoxide, inflammatory cytokines and soluble receptor for advanced glycation end-products (sRAGE). In addition, actein increased the activity of glyoxalase I and levels of reduced glutathione (GSH) and the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2). These findings suggest that actein protects against MG-induced cell damage by reducing oxidative stress and increasing MG detoxification. Treatment with actein prior to MG exposure reduced MG-induced mitochondrial dysfunction by preventing mitochondrial membrane potential dissipation and adenosine triphosphate (ATP) loss. Additionally, peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), nuclear respiratory factor 1 (NRF-1) and nitric oxide (NO) levels were significantly increased by actein, suggesting that actein may induce mitochondrial biogenesis.
  
  
  CONCLUSIONS
  This study demonstrates that actein reduces MG-induced damage in osteoblastic MC3T3-E1 cells by enhancing antioxidant defenses, the glyoxalase system and mitochondrial biogenesis. © 2016 Society of Chemical Industry.
authors.affiliation: Research Institute of Endocrinology, Kyung Hee University Hospital, 1, Hoegi-dong, Dongdaemun-gu, Seoul, 130-702, Republic of Korea.
authors.forename: Kwang Sik
authors.initials: KS
authors.lastname: Suh
authors.affiliation: Department of Endocrinology and Metabolism, School of Medicine, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul, 130-701, Republic of Korea.
authors.forename: Suk
authors.initials: S
authors.lastname: Chon
authors.affiliation: Department of Endocrinology and Metabolism, School of Medicine, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul, 130-701, Republic of Korea.
authors.forename: Eun Mi
authors.initials: EM
authors.lastname: Choi
mesh_terms: D000975:Antioxidants / Q000378:metabolism; D016923:Cell Death / Q000187:drug effects; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D031885:Cimicifuga / Q000737:chemistry; D016207:Cytokines / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D007791:Lactoylglutathione Lyase / Q000378:metabolism; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D051267:NF-E2-Related Factor 2 / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D010006:Osteoblasts / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D018384:Oxidative Stress / Q000187:drug effects*; D011765:Pyruvaldehyde / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D017382:Reactive Oxygen Species / Q000378:metabolism; D000067759:Receptor for Advanced Glycation End Products / Q000378:metabolism; D012503:Saponins / Q000494:pharmacology*; D013481:Superoxides / Q000378:metabolism; D014315:Triterpenes / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D016207:Cytokines; D051267:NF-E2-Related Factor 2; D017382:Reactive Oxygen Species; D000067759:Receptor for Advanced Glycation End Products; D012503:Saponins; D014315:Triterpenes; D013481:Superoxides; D009569:Nitric Oxide; D011765:Pyruvaldehyde; D007791:Lactoylglutathione Lyase; D005978:Glutathione; C096064:actein
keywords: actein; cytotoxicity; methylglyoxal; mitochondrial function; osteoblasts