Abstract
Six new 8-C-p-hydroxybenzylflavonol glycosides were isolated from a hot water extract of pumpkin (Cucurbita moschata Duch.) tendril and elucidated as 8-C-p-hydroxybenzylquercetin 3-O-rutinoside, 8-C-p-hydroxybenzoylquercetin 3-O-β-D-glucopyranoside, 8-C-p-hydroxybenzylkaempferol 3-O-(α-L-rhamnopyranosyl(1→6)-β-D-galactopyranoside, 8-C-p-hydroxybenzoylkaempferol 3-O-rutinoside, 8-C-p-hydroxybenzylisorhamnetin 3-O-rutinoside, and 8-C-p-hydroxybenzylisorhamnetin 3-O-(α-L-rhamnopyranosyl(1→6)-β-D-galactopyranoside. Their chemical structures were determined using nuclear magnetic resonance (NMR) and electrospray ionization-mass spectrometer (ESIMS) analyses. The 8-C-p-hydroxybenzylflavonol glycosides were found to inhibit the receptor activator of nuclear factor-κB (RANKL)-induced osteoclast differentiation of bone marrow derived macrophage (BMDM), an osteoclast progenitor. Additionally, 8-C-p-hydroxybenzylflavonol glycosides effectively reduced the expression of osteoclast-related genes, such as tartrate-resistant acid phosphatase, cathepsin K, nuclear factor activated T-cell cytoplasmic 1, and dendritic cell specific transmembrane protein in RANKL-treated BMDMs. These results indicate that the 8-C-p-hydroxybenzylflavonol glycosides may be the main components responsible for the osteoclast differentiation inhibitory effect of pumpkin tendril.
Highlights
Bone remodeling by osteoblasts, which regulate bone formation, and osteoclasts, which regulate bone resorption, is essential for maintaining bone mass
The proton signals related to the p-hydroxybenzyl moiety were observed at δ 4.05 (2H, s, H-100 ), 7.07 (2H, d, J = 8.4 Hz, H-300 and H-700 ), and 6.64 (2H, d, J = 8.4 Hz, H-400 and H-600 )
The 1 H Nuclear magnetic resonance (NMR) spectrum indicated the presence of β-D-glucopyranose and α-L-rhamnopyranose moieties, including two anomeric proton signals at δ
Summary
Bone remodeling by osteoblasts, which regulate bone formation, and osteoclasts, which regulate bone resorption, is essential for maintaining bone mass. Disruption of the bone formation/resorption balance due to abnormal osteoclast activity leads to skeletal diseases, such as osteoporosis, rheumatoid arthritis, and periodontal disease [1]. Osteoclasts are multinucleated cells differentiated from hematopoietic precursor cells of monocyte/macrophage lineage in the bone marrow. They are characterized by their specialized membrane structures, clear zones and ruffled borders, acid secretion, and lytic enzymes that degrade mineralized bone matrices [2,3]. Osteoclast differentiation and maturation require two critical cytokines, the receptor activator of nuclear factor-kappa B (NF-κB). The binding of RANKL to its receptor activator of NF-κB (RANK) leads to the activation of key transcription factors such as nuclear factor activated T-cell cytoplasmic 1 (NFATc1) [5,6], which enhances osteoclast formation by increasing the expression of osteoclast-related genes [7]. Inhibiting osteoclast differentiation and activation is a key therapeutic strategy for treating bone metabolic diseases
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