Curcumin inhibits the proliferation and mineralization of cultured osteoblasts

Notoya, Michitaka; Nishimura, Hiroyuki; Woo, Je‐Tae; Nagai, Kazuo; Ishihara, Yoko; Hagiwara, Hiromi

doi:10.1016/j.ejphar.2006.01.028

Cited by 58 publications

(41 citation statements)

References 34 publications

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“…It has been reported that the up-regulation of the cyclindependent kinase inhibitor p21 WAF1/CIP1 is involved in the antiproliferative effect of HO-1 [25,37] . CO is one of the products of heme degradation.…”

Section: Discussionmentioning

confidence: 99%

Neferine inhibits angiotensin II-stimulated proliferation in vascular smooth muscle cells through heme oxygenase-1

Tong

Zhang

et al. 2010

Acta Pharmacol Sin

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Aim:To explore the effect of neferine on angiotensin II (Ang II)-induced vascular smooth muscle cell (VSMC) proliferation. Methods: Human umbilical vein smooth muscle cells (HUVSMCs) were used. Cell proliferation was determined by using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis. Heme oxygenase (HO)-1 protein expression was tested by Western blot analysis. Extracellular signal-regulated protein kinase 1/2 (ERK1/2) activation was determined by using immunoblotting. Results: Pre-incubation of HUVSMCs with neferine (0.1, 0.5, 1.0, and 5.0 µmol/L) significantly inhibited Ang II-induced cell proliferation in a concentration-dependent manner and neferine 5.0 µmol/L increased HO-1 expression by 259% compared with control. The antiproliferative effect of neferine was significantly attenuated by coapplication of zinc protoporphyrin IX (ZnPP IX, an HO-1 inhibitor) with neferine. Ang II-enhanced ERK1/2 phosphorylation was markedly reversed by neferine. By inhibiting HO-1 activity with ZnPP IX, the inhibitive effect of neferine on ERK1/2 phosphorylation was significantly attenuated. Cobalt-protoporphyrin (CoPP), an HO-1 inducer, significantly decreased Ang II-induced ERK1/2 phosphorylation and inhibited Ang II-induced cell proliferation. The ERK1/2 pathway inhibitor PD98059 significantly blocked Ang II-enhanced ERK1/2 phosphorylation and inhibited cell proliferation. Conclusion: These findings suggest that neferine can inhibit Ang II-induced HUVSMC proliferation by upregulating HO-1, leading to the at least partial downregulation of ERK1/2 phosphorylation.

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Section: Discussionmentioning

confidence: 99%

Neferine inhibits angiotensin II-stimulated proliferation in vascular smooth muscle cells through heme oxygenase-1

Tong

Zhang

et al. 2010

Acta Pharmacol Sin

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“…Although the inhibition of mineralization by curcumin was observed in the cultured osteoblasts, 15 the calcium content of the distal femur was not decreased by the curcumin supplement in the diabetic rats. This observation probably indicated that curcumin affected the activity and number of osteoclasts rather than osteoblasts.…”

Section: Pathological Bone Environmentmentioning

confidence: 99%

“…15 By contrast, it has recently been investigated that a curcumin analog, UBS109, has a positive role in the differentiation of mouse preosteoblastic MC3T3 cell line by stimulating Smad signaling involved in the activation of bone morphogenetic protein-2. 17 In addition, UBS109 tested in vitro at 10-200 nM stimulates osteoblastic mineralization from bone marrow mesenchymal stem cells, whereas it suppresses the process of adipogenesis of these stem cells.…”

Section: Effects Of Curcumin On Bonementioning

confidence: 99%

“…Using 5-10 mM treatment, Notoya et al 15 demonstrated the inhibitory effects of curcumin on proliferation of osteoblasts derived from calvaria of rats (ROB) without inducing apoptosis.This effect might result from the arrest of cell cycle progression via expression of p21 protein. In contrast, Chan et al 16 reported that curcumin induced two distinct cell death programs in osteoblasts according to its concentration.…”

Section: Effects Of Curcumin On Bonementioning

confidence: 99%

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Therapeutic actions of curcumin in bone disorders

2016

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Curcumin is the active component of turmeric extract derived from the Curcuma longa plant. In the last decade, curcumin has raised a considerable interest in medicine owing to its negligible toxicity and multiple therapeutic actions including anti-cancer, anti-inflammatory and anti-microbial activities. Among the various molecular targets of curcumin, some are involved in bone remodeling, which strongly suggests that curcumin can affect the skeletal system. The review sheds light on the current and potential applications of curcumin to treat bone disorders characterized by an excessive resorption activity. Within the scope of this review, the novel formulations of curcumin to overcome its physico-chemical and pharmacokinetic constraints are also discussed.

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“…CM acts on multiple targets and inhibits activation of key cell signaling mediators, including NFκB, AP-1, Cox-2, MMP9, and EGFR (Shishodia et al, 2007). In breast cancer cells, CM's antiproliferative effects have been linked to apoptosis induction and regulates p21 expression through a p53-dependent pathway (Notoya et al, 2006;Park et al, 2002;Zheng and Chen, 2004;Choudhuri et al, 2005;Aggarwal et al, 2007;Gao et al, 2012). Despite a difficult in understanding the cell biological processes underlying cancer, there are few effective therapies, emphasizing the need for new insights into this disorder.…”

Section: Introductionmentioning

confidence: 99%