title: Inhibitory effect of apocynin on methylglyoxal-mediated glycation in osteoblastic MC3T3-E1 cells.
abstract: Methylglyoxal (MG), a highly reactive metabolite of hyperglycemia, can enhance protein glycation, oxidative stress or inflammation. The present study investigated the effects of apocynin on the mechanisms associated with MG toxicity in osteoblastic MC3T3-E1 cells. Pretreatment of MC3T3-E1 cells with apocynin prevented the MG-induced protein glycation and formation of intracellular reactive oxygen species and mitochondrial superoxide in MC3T3-E1 cells. In addition, apocynin increased glutathione levels and restored the activity of glyoxalase I inhibited by MG. These findings suggest that apocynin provide a protective action against MG-induced cell damage by reducing oxidative stress and by increasing the MG detoxification system. Apocynin treatment decreased the levels of proinflammatory cytokines such as tumor necrosis factor-α and interleukin-6 induced by MG. Additionally, the nitric oxide level reduced by MG was significantly increased by apocynin. These findings indicate that apocynin might exert its therapeutic effects via upregulation of glyoxalase system and antioxidant activity. Taken together, apocynin may prove to be an effective treatment for diabetic osteopathy.
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.forename: Sang Youl
authors.initials: SY
authors.lastname: Rhee
authors.forename: Young Seol
authors.initials: YS
authors.lastname: Kim
authors.forename: Eun Mi
authors.initials: EM
authors.lastname: Choi
mesh_terms: D016475:3T3 Cells; D000098:Acetophenones / Q000494:pharmacology*; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D002470:Cell Survival / Q000187:drug effects; D002999:Clone Cells; D016207:Cytokines / Q000037:antagonists & inhibitors / Q000378:metabolism; D005978:Glutathione / Q000819:agonists / Q000378:metabolism; D017127:Glycation End Products, Advanced / Q000819:agonists / Q000037:antagonists & inhibitors* / Q000378:metabolism; D006031:Glycosylation / Q000187:drug effects; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007791:Lactoylglutathione Lyase / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000235:genetics; D051379:Mice; D008928:Mitochondria / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D009569:Nitric Oxide / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism; D010006:Osteoblasts / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D011765:Pyruvaldehyde / Q000037:antagonists & inhibitors* / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000037:antagonists & inhibitors / Q000378:metabolism; D013481:Superoxides / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D000098:Acetophenones; D000894:Anti-Inflammatory Agents, Non-Steroidal; D016207:Cytokines; D017127:Glycation End Products, Advanced; D007004:Hypoglycemic Agents; D017382:Reactive Oxygen Species; D013481:Superoxides; D009569:Nitric Oxide; D011765:Pyruvaldehyde; C056165:acetovanillone; C000597198:GLOD1 protein, mouse; D007791:Lactoylglutathione Lyase; D005978:Glutathione
keywords: apocynin; glycation; glyoxalase; methylglyoxal; osteoblasts