NDLI: Luteolin alleviates methylglyoxal-induced cytotoxicity in osteoblastic MC3T3-E1 cells.

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Luteolin alleviates methylglyoxal-induced cytotoxicity in osteoblastic MC3T3-E1 cells.

Content Provider	Europe PMC
Author	Suh, Kwang Sik Chon, Suk Choi, Eun Mi
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.
Related Links	https://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC5101326&blobtype=pdf
ISSN	09209069
Volume Number	68
DOI	10.1007/s10616-016-9977-y
PubMed Central reference number	PMC5101326
Issue Number	6
PubMed reference number	27221336
Journal	Cytotechnology
e-ISSN	15730778
Language	English
Publisher	Springer Netherlands
Publisher Date	2016-05-24
Publisher Place	Dordrecht
Access Restriction	Open
Rights License	© Springer Science+Business Media Dordrecht 2016
Subject Keyword	Reactive oxygen species Glutathione Osteoblasts Nitric oxide Mitochondrial function
Content Type	Text
Resource Type	Article
Subject	Cell Biology Clinical Biochemistry Bioengineering Biomedical Engineering Biotechnology

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