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Tytuł pozycji:

Zanthoxylum piperitum alleviates the bone loss in osteoporosis via inhibition of RANKL-induced c-fos/NFATc1/NF-κB pathway.

Tytuł:
Zanthoxylum piperitum alleviates the bone loss in osteoporosis via inhibition of RANKL-induced c-fos/NFATc1/NF-κB pathway.
Autorzy:
Kim MH; Department of Convergence Korean Medical Science, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Lee H; Department of Convergence Korean Medical Science, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Ha IJ; Korean Medicine Clinical Trial Center, Kyung Hee University Korean Medicine Hospital, Kyung Hee University, Seoul, South Korea.
Yang WM; Department of Convergence Korean Medical Science, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea. Electronic address: .
Źródło:
Phytomedicine : international journal of phytotherapy and phytopharmacology [Phytomedicine] 2021 Jan; Vol. 80, pp. 153397. Date of Electronic Publication: 2020 Oct 22.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Publication: Stuttgart : Urban & Fischer Verlag
Original Publication: Stuttgart ; New York : G. Fischer, c1994-
MeSH Terms:
Osteoclasts/*drug effects
Osteoporosis/*drug therapy
Plant Extracts/*pharmacology
Zanthoxylum/*chemistry
Animals ; Bone Density/drug effects ; Bone Resorption/drug therapy ; Bone Resorption/metabolism ; Female ; Mice ; Mice, Inbred ICR ; NF-kappa B/metabolism ; NFATC Transcription Factors/metabolism ; Osteoclasts/metabolism ; Osteoporosis/etiology ; Osteoporosis/metabolism ; Ovariectomy/adverse effects ; Proto-Oncogene Proteins c-fos/metabolism ; RANK Ligand/metabolism ; RAW 264.7 Cells
Contributed Indexing:
Keywords: Bone mineral density; Osteoclast; Osteoporosis; RANKL; Zanthoxylum piperitum
Substance Nomenclature:
0 (NF-kappa B)
0 (NFATC Transcription Factors)
0 (Nfatc1 protein, mouse)
0 (Plant Extracts)
0 (Proto-Oncogene Proteins c-fos)
0 (RANK Ligand)
0 (Tnfsf11 protein, mouse)
Entry Date(s):
Date Created: 20201101 Date Completed: 20210115 Latest Revision: 20220418
Update Code:
20240105
DOI:
10.1016/j.phymed.2020.153397
PMID:
33130475
Czasopismo naukowe
Background: The fruit of Zanthoxylum piperitum (ZP) is an herbal medicine as well as a spice agent in Asia to treat carminative, stomachic, anthelmintic and degenerative diseases. Z. piperitum was reported to have anti-oxidant, anti-inflammatory, anti-osteoarthritic and osteosarcoma proliferation-control effects.
Purpose and Study Design: This study was conducted to determine the anti-osteoporotic effects and mechanisms of action of ZP.
Methods: Female ICR mice underwent ovariectomies (OVX) and were orally administered ZP at 1, 10 and 100 mg/kg for 6 weeks. The femoral and tibial bones were assessed by dual-energy X-ray absorptiometry and histology to analyze the bone mineral density (BMD) and the number of osteoclasts. Raw 264.7 cells were stimulated by 100 ng/ml receptor activator of nuclear factor-κB ligand (RANKL) for 7 days in the presence of ZP. RANKL-induced signaling molecules were analyzed in osteoclasts.
Results: The levels of femoral and tibial BMD were significantly increased by ZP administration. Serum biomarkers such as osteocalcin, calcium, alkaline phosphatase and bone-specific alkaline phosphatase concentrations were markedly recovered to normal levels in ZP-treated osteoporotic mice. In addition, the number of osteoclasts in the head, trochanter and body of the femur was obviously decreased in the ZP treatment groups. Moreover, ZP treated-cells showed a reduction in the number of TRAP-positive multinuclear cells in RANKL-stimulated Raw 264.7 cells. ZP decreased the RANKL-activated NFATc1 and c-fos, transcription factors of osteoclast formation. The nuclear translocation of NF-κB and phosphorylation of ERK42/44 were inhibited by the ZP treatment in RANKL-induced osteoclasts.
Conclusion: Collectively, ZP exerts its inhibitory effect against bone resorption by regulating RANKL-mediated c-fos/NFATc1/NF-κB in osteoclast. ZP may prove to be a therapeutic agent for osteoporosis.
(Copyright © 2020. Published by Elsevier GmbH.)

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