Study of the mechanisms by which Sambucus williamsii HANCE extract exert protective effects against ovariectomy-induced osteoporosis in vivo.
The purpose of this study is to investigate the dose-dependent effects of SWH on bone properties and the mechanism involved in mediating the osteoprotective actions of SWH. The results indicated that SWH could improve bone properties by inhibiting the process of bone resorption and stimulating the process of bone formation.


BACKGROUND
Our previous study showed that Sambucus williamsii HANCE (SWH) improved trabecular bone mass and cortical bone strength in ovariectomized (OVX) rats. The purpose of this study is to investigate the dose-dependent effects of SWH on bone properties and the mechanism involved in mediating the osteoprotective actions of SWH.


METHODS
Three-month-old C57BL/6J mice were fed a phytoestrogen-free diet and subjected to either ovariectomy or sham operation. OVX mice were treated with genistein (50 mg/kg), or a low (200 mg/kg), medium (500 mg/kg), or high (1,000 mg/kg) dose of SWH extract.


RESULTS
SWH could dose-dependently decrease urinary Ca excretion and increase serum Ca level in OVX mice. It could increase tibial bone mineral density and exert beneficial effects on the microarchitecture of trabecular bone in the OVX mice. SWH suppressed the ovariectomy-induced expression of Cbfa1 mRNA and cathepsin K mRNA and enhanced the ratio of OPG/RANKL mRNA expression in the tibia. In vitro study showed that SWH dramatically reduced the number of TRAP-positive cells in RANKL-induced RAW 264.7 cells.


CONCLUSIONS
The present study indicated that SWH could improve bone properties by inhibiting the process of bone resorption and stimulating the process of bone formation.
Zhang
Y
Y
Center of System Biomedical Sciences, University of Shanghai for Science and Technology, Shanghai, 200093, People's Republic of China.
Li
Q
Q
Wan
H-Y
HY
Xiao
H-H
HH
Lai
W-P
WP
Yao
X-S
XS
Wong
M-S
MS
D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D015519:Bone Density / Q000187:drug effects; D001862:Bone Resorption / Q000378:metabolism*; D002118:Calcium / Q000097:blood / Q000378:metabolism; D016022:Case-Control Studies; D056657:Cathepsin K / Q000378:metabolism; D002460:Cell Line; D050659:Core Binding Factor Alpha 1 Subunit / Q000187:drug effects / Q000378:metabolism; D005136:Eye Proteins / Q000187:drug effects / Q000378:metabolism; D005260:Female; D006614:Hindlimb; D018398:Homeodomain Proteins / Q000187:drug effects / Q000378:metabolism; D007527:Isoenzymes / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D010024:Osteoporosis / Q000188:drug therapy*; D053244:Osteoprotegerin / Q000187:drug effects / Q000378:metabolism; D010052:Ovariectomy; D010936:Plant Extracts / Q000494:pharmacology*; D053245:RANK Ligand / Q000378:metabolism; D027923:Sambucus; D000071681:Tartrate-Resistant Acid Phosphatase; D013977:Tibia; D014157:Transcription Factors / Q000187:drug effects / Q000378:metabolism; D016896:Treatment Outcome
D050659:Core Binding Factor Alpha 1 Subunit; D005136:Eye Proteins; D018398:Homeodomain Proteins; D007527:Isoenzymes; D053244:Osteoprotegerin; D010936:Plant Extracts; D053245:RANK Ligand; C105441:Rax protein, mouse; C493716:Runx2 protein, mouse; C506031:Tnfrsf11b protein, mouse; D014157:Transcription Factors; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase; D056657:Cathepsin K; D002118:Calcium