title: Luteolin alleviates methylglyoxal-induced cytotoxicity in osteoblastic MC3T3-E1 cells.
abstract: Methylglyoxal (MG), a reactive sugar-derived metabolite, exerts harmful effects by inducing oxidative stress, which aggravates a series of diabetic complications, including osteoporosis. The present study was performed to examine the effects of luteolin, a dietary polyphenolic flavonoid, on MG-induced cytotoxicity in MC3T3-E1 osteoblastic cells. Pretreatment of MC3T3-E1 osteoblastic cells with luteolin prevented MG-induced cell death and production of tumor necrosis factor-alpha, intracellular reactive oxygen species, mitochondrial superoxide, and cardiolipin peroxidation. In addition, luteolin increased the levels of glutathione and nuclear factor erythroid 2-related factor 2 (Nrf2) and decreased the inhibition of heme oxygenase-1 activity by MG. Pretreatment with luteolin prior to MG exposure reduced MG-induced mitochondrial dysfunction and increased the peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) and nitric oxide levels, suggesting that luteolin may induce mitochondrial biogenesis. Taken together, these observations indicated that luteolin has potential as a preventive agent against the development of diabetic osteopathy related to MG-induced oxidative stress in diabetes.
authors.affiliation: Research Institute of Endocrinology, Kyung Hee University Hospital, 1, Hoegi-dong, Dongdaemun-gu, Seoul, 130-702, South 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, South 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, South Korea. cheunmi@hanmail.net.
authors.forename: Eun Mi
authors.initials: EM
authors.lastname: Choi
keywords: Glutathione; Mitochondrial function; Nitric oxide; Osteoblasts; Reactive oxygen species