Exploring the Anti-Osteoporotic Potential of Daucosterol: Impact on Osteoclast and Osteoblast Activities.
bone metabolism
daucosterol
osteoblast
osteoclast
osteoporosis
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
17 Nov 2023
17 Nov 2023
Historique:
received:
27
10
2023
revised:
14
11
2023
accepted:
15
11
2023
medline:
27
11
2023
pubmed:
25
11
2023
entrez:
25
11
2023
Statut:
epublish
Résumé
Osteoporosis is a debilitating condition characterized by reduced bone mass and density, leading to compromised structural integrity of the bones. While conventional treatments, such as bisphosphonates and selective estrogen receptor modulators (SERMs), have been employed to mitigate bone loss, their effectiveness is often compromised by a spectrum of adverse side effects, ranging from gastrointestinal discomfort and musculoskeletal pain to more severe concerns like atypical fractures and hormonal imbalances. Daucosterol (DC), a natural compound derived from various plant sources, has recently garnered considerable attention in the field of pharmacology. In this study, we investigated the anti-osteoporosis potential of DC by characterizing its role in osteoclasts, osteoblasts, and lipopolysaccharide (LPS)-induced osteoporosis. The inhibitory effect of DC on osteoclast differentiation was determined by tartrate-resistant acid phosphatase (TRAP) staining, F-actin ring formation by fluorescent staining, and bone resorption by pit formation assay. In addition, the calcification nodule deposition effect of osteoblasts was determined by Alizarin red S staining. The effective mechanisms of both cells were verified by Western blot and reverse transcription polymerase chain reaction (RT-PCR). To confirm the effect of DC in vivo, DC was administered to a model of osteoporosis by intraperitoneal administration of LPS. The anti-osteoporosis effect was then characterized by micro-CT and serum analysis. The results showed that DC effectively inhibited osteoclast differentiation at an early stage, promoted osteoblast activity, and inhibited LPS-induced bone density loss. The results of this study suggest that DC can treat osteoporosis through osteoclast and osteoblast regulation, and therefore may be considered as a new therapeutic alternative for osteoporosis patients in the future.
Identifiants
pubmed: 38003654
pii: ijms242216465
doi: 10.3390/ijms242216465
pmc: PMC10671633
pii:
doi:
Substances chimiques
lyoniside
U45VN859W3
Lipopolysaccharides
0
RANK Ligand
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Ministry of Education
ID : 2022R1I1A1A01063801
Organisme : Korea Health Industry Development Institute
ID : HF21C0092
Pays : Republic of Korea
Références
Int J Mol Sci. 2019 Apr 04;20(7):
pubmed: 30987410
J Nephropharmacol. 2015 Jan 01;4(1):27-30
pubmed: 28197471
Biochem Biophys Res Commun. 2006 Dec 8;351(1):99-105
pubmed: 17052691
Trends Mol Med. 2006 Jan;12(1):17-25
pubmed: 16356770
Endocrinology. 2002 Aug;143(8):3105-13
pubmed: 12130576
Calcif Tissue Int. 1998 Apr;62(4):332-40
pubmed: 9504959
Biochem Biophys Res Commun. 2009 Jan 2;378(1):1-5
pubmed: 18992710
Biochem Biophys Res Commun. 2017 Aug 5;489(4):472-476
pubmed: 28576497
J Cell Physiol. 2001 Jul;188(1):89-97
pubmed: 11382925
Nutrients. 2023 Jan 01;15(1):
pubmed: 36615880
Autoimmunity. 2008 Apr;41(3):218-23
pubmed: 18365835
Life Sci. 2015 Sep 15;137:37-43
pubmed: 26209138
Nature. 2003 May 15;423(6937):337-42
pubmed: 12748652
World J Orthop. 2012 Dec 18;3(12):212-22
pubmed: 23362465
Front Endocrinol (Lausanne). 2015 Feb 16;6:15
pubmed: 25762979
Eur J Endocrinol. 2011 Jul;165(1):1-10
pubmed: 21543379
Bioelectromagnetics. 2016 Apr;37(3):152-162
pubmed: 26891468
Vaccine. 2007 May 10;25(19):3834-40
pubmed: 17335944
J Ethnopharmacol. 2020 Jan 30;247:112251
pubmed: 31560992
J Bone Miner Res. 2003 Jul;18(7):1198-205
pubmed: 12854829
Toxicology. 2022 Jan 15;465:153053
pubmed: 34838596
Front Physiol. 2021 Jan 05;11:511799
pubmed: 33584321
Cells. 2020 Sep 10;9(9):
pubmed: 32927921
J Drug Target. 2022 Apr;30(4):394-412
pubmed: 34859718
J Clin Invest. 2013 Feb;123(2):666-81
pubmed: 23321671
Connect Tissue Res. 2018 Mar;59(2):99-107
pubmed: 28324674
Med Decis Making. 2016 Nov;36(8):1011-9
pubmed: 26683247
Exp Cell Res. 2007 Jan 1;313(1):168-78
pubmed: 17084841
Eur J Pharmacol. 2015 Jul 15;759:287-94
pubmed: 25814262
J Bone Miner Metab. 2006;24(5):355-8
pubmed: 16937266
Arch Pharm Res. 2012 Dec;35(12):2143-6
pubmed: 23263808
Adv Exp Med Biol. 2010;658:43-9
pubmed: 19950014
J Biomed Mater Res A. 2017 Sep;105(9):2510-2521
pubmed: 28509410
J Cell Sci. 2012 Jun 15;125(Pt 12):2910-7
pubmed: 22454522
Med Sci Monit Basic Res. 2016 Sep 26;22:95-106
pubmed: 27667570
J Bone Metab. 2014 Nov;21(4):233-41
pubmed: 25489571
Clin Cases Miner Bone Metab. 2017 May-Aug;14(2):209-216
pubmed: 29263736
Science. 1994 Oct 21;266(5184):443-8
pubmed: 7939685
Science. 2000 Sep 1;289(5484):1504-8
pubmed: 10968780
Expert Rev Clin Pharmacol. 2011 Sep;4(5):593-604
pubmed: 22220306
J Bone Miner Res. 2001 Jul;16(7):1228-36
pubmed: 11450698
Mol Endocrinol. 2008 Jan;22(1):176-85
pubmed: 17885208
Molecules. 2017 Jun 02;22(6):
pubmed: 28574485
Biomed Pharmacother. 2019 Jul;115:108916
pubmed: 31054506
J Cell Physiol. 2007 Jun;211(3):728-35
pubmed: 17226753
Bone. 2020 Mar;132:115220
pubmed: 31904537
J Bone Miner Res. 2009 May;24(5):871-85
pubmed: 19113919
Gene. 2004 Oct 27;341:19-39
pubmed: 15474285