title: Inhibitory effect of paeoniflorin on methylglyoxal-mediated oxidative stress in osteoblastic MC3T3-E1 cells.
abstract: OBJECTIVE
  Methylglyoxal (MG) has been suggested to be one major source of intracellular reactive carbonyl compounds. In the present study, the effect of paeoniflorin on MG-induced cytotoxicity was investigated using osteoblastic MC3T3-E1 cells.
  
  
  METHODS
  Osteoblastic MC3T3-E1 cells were pre-incubated with paeoniflorin before treatment with MG, and markers of oxidative damage and mitochondrial function were examined.
  
  
  RESULTS
  Pretreatment of MC3T3-E1 cells with paeoniflorin prevented the MG-induced cell death and formation of intracellular reactive oxygen species, cardiolipin peroxidation, and protein adduct in osteoblastic MC3T3-E1 cells. In addition, paeoniflorin increased glutathione level and restored the activity of glyoxalase I to almost the control level. These findings suggest that paeoniflorin provide a protective action against MG-induced cell damage by reducing oxidative stress and by increasing MG detoxification system. Pretreatment with paeoniflorin prior to MG exposure reduced MG-induced mitochondrial dysfunction by preventing mitochondrial membrane potential dissipation and adenosine triphosphate loss. Additionally, the nitric oxide and nuclear respiratory factor 1 levels were significantly increased by paeoniflorin, suggesting that paeoniflorin may induce mitochondrial biogenesis. Paeoniflorin treatment decreased the levels of proinflammatory cytokines such as TNF-α and IL-6.
  
  
  CONCLUSIONS
  These findings indicate that paeoniflorin might exert its therapeutic effects via upregulation of glyoxalase system and mitochondrial function. Taken together, paeoniflorin may prove to be an effective treatment for diabeteic osteopathy.
authors.affiliation: Department of Food & Nutrition, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea. Electronic address: cheunmi@hanmail.net.
authors.forename: Eun Mi
authors.initials: EM
authors.lastname: Choi
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 & Metabolism, School of Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.
authors.forename: Sang Youl
authors.initials: SY
authors.lastname: Rhee
authors.affiliation: Department of Endocrinology & Metabolism, School of Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.
authors.forename: Young Seol
authors.initials: YS
authors.lastname: Kim
mesh_terms: D000818:Animals; D002308:Cardiolipins / Q000378:metabolism; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D005786:Gene Expression Regulation / Q000187:drug effects*; D005960:Glucosides / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D015227:Lipid Peroxidation; D051379:Mice; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D039821:Monoterpenes / Q000494:pharmacology*; D009569:Nitric Oxide / Q000378:metabolism; D010006:Osteoblasts / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects*; D011765:Pyruvaldehyde / Q000009:adverse effects; D017382:Reactive Oxygen Species / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D006027:Glycosides
chemical_list: D002308:Cardiolipins; D005960:Glucosides; D005978:Glutathione; D015850:Interleukin-6; D039821:Monoterpenes; D009569:Nitric Oxide; D011765:Pyruvaldehyde; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; C577686:interleukin-6, mouse; C015423:peoniflorin; D006027:Glycosides
keywords: Cytotoxicity; Methylglyoxal; Mitochondrial function; Osteoblasts; Paeoniflorin