ReferenceID 5118

Antiosteoporosis and bone protective effect of dieckol against glucocorticoid-induced osteoporosis in rats

Front Endocrinol (Lausanne)

Background: Glucocorticoids (GCs) induce osteoporosis, which results in fractures in the bond, causing significant morbidity. In the conducted study, we examined the antiosteoporosis effect of dieckol against GC-induced

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Reference Id
5118
Evidence Id
21708
Core Evidence Id
21708
Source Reference Id
3522
Herb2 Reference Id
HBREF004319
Subject Paper Key
HBIN023738_36060953
Pubmed Id
36060953
Doi
10.3389/fendo.2022.932488
Paper Title
Antiosteoporosis and bone protective effect of dieckol against glucocorticoid-induced osteoporosis in rats
Paper Abstract
Background: Glucocorticoids (GCs) induce osteoporosis, which results in fractures in the bond, causing significant morbidity. In the conducted study, we examined the antiosteoporosis effect of dieckol against GC-induced osteoporosis in rats. Methods: Sprague-Dawley (SD) rats were used for the current study and dexamethasone (2.5 mg/kg) induced osteoporosis in the rats that received the dieckol (test) and alendronate (standard) for 20 weeks. Bone turnover parameters, microCT, antioxidant, inflammatory cytokines, nutrient, and hormones parameters. Results: Dieckol noticeably suppressed the body weight and boosted the uterine and vagina weight. Dieckol considerably altered the level of trabecular number (Tb. N), the bone volume to total volume (BV/TV), trabecular separation (Tb.Sp), bone surface to bone volume (BS/BV), and t​r​a​b​e​c​u​l​a​r thickness (Tb.Th). Dieckol noticeably (P < 0.001) elevated the level of osteocalcin (OC) and alleviated the level of bone Gla protein (BGP), acid phosphatase (ACP), alkaline phosphatase (ALP), and β-CTx. Dieckol markedly boosted the level of malondialdehyde (MDA) and suppressed the level of glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) along with the suppression of inflammatory cytokines like TNF-α, IL-1β, and IL-6. Dieckol remarkably increased the level of calcium, potassium, magnesium, and 25 (OH) vitamin D. Dieckol substantially (P < 0.001) boosted the level of estradiol and alleviated the level of parathyroid hormone and tartrate-resistant acid phosphatase (TRAP). Dieckol also suppressed the level of receptor activator of nuclear factor κB ligand (RANKL) and boosted the level of osteoprotegerin (OPG). Conclusion: Taken together, our data suggest that dieckol demonstrated the anti-osteoporosis effect against GC-induced osteoporosis in rats.
Journal
Front Endocrinol (Lausanne)
Publish Year
2022
Experiment Subject
rat
Experiment Type
Animal Experiment
Phenotype Related
Osteoporosis
Paper Title Cn
Paper Title En
Antiosteoporosis and bone protective effect of dieckol against glucocorticoid-induced osteoporosis in rats
Bilingual Status
semi_complete