Modulatory effects of luteolin on osteoblastic function and inflammatory mediators in osteoblastic MC3T3-E1 cells

• Published in: Cell biology international Vol. 31; no. 9; pp. 870 - 877
• Main Author: Choi, Eun-Mi
• Format: Journal Article
• Language: English
• Published: Oxford, UK Elsevier Ltd 01.09.2007; Blackwell Publishing Ltd
• Subjects: Acetonitriles - pharmacology; Alkaline Phosphatase - metabolism; Animals; Cell Line; Collagen - biosynthesis; Dinoprostone - biosynthesis; Inflammation Mediators - metabolism; Interleukin-6 - biosynthesis; Luteolin; Luteolin - chemistry; Luteolin - pharmacology; Mice; Morpholines - pharmacology; Nitric Oxide - biosynthesis; Osteoblastic MC3T3-E1 cells; Osteoblasts - drug effects; Osteoblasts - metabolism; Osteoblasts - secretion; Osteocalcin - secretion; Phytoestrogens - chemistry; Tumor Necrosis Factor-alpha - biosynthesis; Osteoblastic MC3T3-E1 cells; Luteolin
• ISSN: 1065-6995; 1095-8355
• DOI: 10.1016/j.cellbi.2007.01.038

The effects of luteolin on the function of osteoblastic MC3T3-E1 cells and the production of local factors in osteoblasts were investigated. Luteolin (1 μM) caused a significant elevation of collagen content, alkaline phosphatase (ALP) activity, and osteocalcin secretion in the cells ( P < 0.05). The effect of luteolin in increasing collagen content and ALP activity was completely prevented by the presence of 10 −6 M cycloheximide and 10 −6 M tamoxifen, suggesting that luteolin's effect results from a newly synthesized protein component and might be partly involved in estrogen action. We then examined the effect of luteolin on the 3-morpholinosydnonimine (SIN-1)-induced production of oxidative stress markers [nitric oxide (NO) and prostaglan E 2 (PGE 2)] and cytokines [tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6)] in osteoblasts. Luteolin (1 and 10 μM) decreased the SIN-1-induced production of NO, PGE 2, TNF-α, and IL-6 in osteoblasts. These results suggest that inflammatory mediators can be regulated by luteolin stimulating osteoblastic function.