The anti-osteoporotic activity of amine-carboxyboranes in rodents

Kg, Rajendran; Sy, Chen; Sood, Anup; Bf, Spielvogel; Hall, I. H.

doi:10.1016/0753-3322(96)82606-0

Cited by 37 publications

(26 citation statements)

References 39 publications

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“…Lipids have been shown to accumulate in bones of rats and blood vessels around bone in patients with osteo porosis [22,23] . Osteoporosis has been associated with both atherosclerosis and vascular calcification [24][25][26] .…”

Section: Discussionmentioning

confidence: 99%

High cholesterol diet increases osteoporosis risk via inhibiting bone formation in rats

Sheng

Tang

et al. 2011

Acta Pharmacol Sin

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Aim: To investigate the effects of high cholesterol diet on the development of osteoporosis and the underlying mechanisms in rats. Methods: Female Sprague-Dawley rats were randomly separated into 3 groups: (1) the high cholesterol fed rats were fed a high cholesterol diet containing 77% normal diet food, 3% cholesterol and 20% lard for 3 months; (2) ovariectomised (OVX) rats were bilaterally ovariectomised and fed a standard diet; and (3) the control rats were fed the standard diet. Bone mineral density (BMD) of the rats was measured using dual-energy X-ray absorptiometry. Serum levels of oestradiol (E2), osteocalcin (BGP) and carboxy-terminal collagen crosslinks (CTX) were measured using ELISA. Gene expression profile was determined with microarray. Mouse osteoblast cells (MC3T3-E1) were used for in vitro study. Proliferation, differentiation and oxidative stress of the osteoblasts were investigated using MTT, qRT-PCR and biochemical methods. Results: In high cholesterol fed rats, the femur BMD and serum BGP level were significantly reduced, while the CTX level was significantly increased. DNA microarray analysis showed that 2290 genes were down-regulated and 992 genes were up-regulated in this group of rats. Of these genes, 1626 were also down-regulated and 1466 were up-regulated in OVX rats. In total, 370 genes were up-regulated in both groups, and 976 genes were down-regulated. Some of the down-regulated genes were found to code for proteins involved in the transforming growth factor beta (TGF-β)/bone morphogenic protein (BMP) and Wnt signaling pathways. The up-regulated genes were found to code for IL-6 and Ager with bone-resorption functions. Treatment of MC3T3-E1 cells with cholesterol (12.5-50 μg/mL) inhibited the cell proliferation and differentiation in vitro in a concentration-dependent manner. The treatment also concentration-dependently reduced the expression of BMP2 and Cbfa1, and increased the oxidative injury in MC3T3-E1 cells. Conclusion:The results suggest a close correlation between hypercholesterolaemia and osteoporosis. High cholesterol diet increases the risk of osteoporosis, possible via inhibiting the differentiation and proliferation of osteoblasts.

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Section: Discussionmentioning

confidence: 99%

High cholesterol diet increases osteoporosis risk via inhibiting bone formation in rats

Sheng

Tang

et al. 2011

Acta Pharmacol Sin

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“…It was shown that lipids accumulate around bone vessels [16]. Parhami et al found that oxidized lipids and hyperlipidemia may inhibit osteoblastic differentiation [17].…”

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confidence: 98%

The Possible Association between Serum Cholesterol Concentration and Decreased Bone Mineral Density as well as Intravertebral Marrow Fat in HIV-1 Infected Patients

et al. 2007

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“…16,18 Lipids have been shown to accumulate in bones of mice and around bone vessels in patients with osteoporosis. 19,20 Because the immature osteoblasts are located immediately adjacent to the subendothelial matrix of bone vessels, lipid accumulation in subendothelial matrix would be expected to inhibit differentiation of the bone-forming cells. In addition, because oxidized lipids induce endothelial expression of monocyte chemotactic factors and M-CSF, a potent inducer of osteoclastic differentiation, oxidized lipids would be expected to promote bone resorption by recruitment and differentiation of osteoclast precursor cells.…”

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confidence: 99%

Role of Lipids in Osteoporosis

Parhami¹,

Garfinkel²,

Demer³

2000

ATVB

169

105

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Abstract-Cardiovascular disease and osteoporosis together account for most of the morbidity and mortality in our aging population despite significant improvements in treatment. Recently, converging lines of evidence suggest that these 2 diseases share an etiologic factor -that hyperlipidemia contributes not only to atherosclerotic plaque formation, but also to osteoporosis, following a similar biologic mechanism involving lipid oxidation. In vitro studies indicate that lipid products of oxidation promote osteoblastic differentiation of vascular cells and inhibit such differentiation in bone cells. [1][2][3][4][5][6][7][8][9] Although this association is often dismissed as a consequence of aging, the relationship remains significant after age adjustment in some 1,9 but not all 10 studies. Osteoporotic postmenopausal women are at significantly greater risk for cardiovascular disease than agematched controls. 11 Patients with lower bone density and osteoporosis also have higher lipid levels, more severe coronary atherosclerosis, and have a greater risk of stroke death. 2,3,[12][13][14][15] The common finding of simultaneous vascular calcification and osteoporosis in individual patients suggests that local tissue factors govern regulation of biomineralization.Bone and vascular tissue share several features at the molecular and cellular levels. Bone and marrow both contain endothelial cells, preosteoblasts, and monocyte-derived osteoclasts, all of which have counterparts in the artery wall. Both bone and atherosclerotic arteries contain osteopontin, bone morphogenetic protein, matrix Gla protein, collagen I, osteonectin, osteocalcin, nitric oxide, and matrix vesicles. Atherosclerosis and osteoporosis both involve recruitment and differentiation of monocytic cells that differentiate into macrophage-foam cells in artery and osteoclasts in bone. Each cylindrical unit of bone, the osteon, contains a central vessel lined with endothelial cells and a subendothelial matrix. Osteoblast progenitor cells are located immediately outside this matrix.The artery wall contains cells capable of differentiation into osteoblasts, following the same stages of differentiation as occur in bone-derived osteoblasts, and ultimately producing bone mineral. 16 The same oxidized lipids that induce atherosclerosis also induce mineralization and differentiation of the osteoblastic cells in the artery wall. 16 Consistent with this finding, hyperlipidemia is associated with vascular calcification in mice. 17 However, in bone and bone osteoblasts, osteoblastic differentiation is inhibited by oxidized lipids and hyperlipidemia. 16,18 Lipids have been shown to accumulate in bones of mice and around bone vessels in patients with osteoporosis. 19,20 Because the immature osteoblasts are located immediately adjacent to the subendothelial matrix of bone vessels, lipid accumulation in subendothelial matrix would be expected to inhibit differentiation of the bone-forming cells. In addition, because oxidized lipids induce endothelial expression of monocyte ...

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The anti-osteoporotic activity of amine-carboxyboranes in rodents

Cited by 37 publications

References 39 publications

High cholesterol diet increases osteoporosis risk via inhibiting bone formation in rats

High cholesterol diet increases osteoporosis risk via inhibiting bone formation in rats

The Possible Association between Serum Cholesterol Concentration and Decreased Bone Mineral Density as well as Intravertebral Marrow Fat in HIV-1 Infected Patients

Role of Lipids in Osteoporosis

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