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

BackgroundGlucocorticoids (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.MethodsSprague–Dawley (SD) rats were used for the current stu...

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Main Authors: Hao Wang, Leigang Yang, Junwei Chao
Format: Article
Language:English
Published: Frontiers Media S.A. 2022-08-01
Series:Frontiers in Endocrinology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fendo.2022.932488/full
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author Hao Wang
Leigang Yang
Junwei Chao
author_facet Hao Wang
Leigang Yang
Junwei Chao
author_sort Hao Wang
collection DOAJ
description BackgroundGlucocorticoids (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.MethodsSprague–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.ResultsDieckol 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).ConclusionTaken together, our data suggest that dieckol demonstrated the anti-osteoporosis effect against GC-induced osteoporosis in rats.
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spelling doaj.art-776df7a0395c49fda84245f0957f45202022-12-22T03:59:18ZengFrontiers Media S.A.Frontiers in Endocrinology1664-23922022-08-011310.3389/fendo.2022.932488932488Antiosteoporosis and bone protective effect of dieckol against glucocorticoid-induced osteoporosis in ratsHao WangLeigang YangJunwei ChaoBackgroundGlucocorticoids (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.MethodsSprague–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.ResultsDieckol 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).ConclusionTaken together, our data suggest that dieckol demonstrated the anti-osteoporosis effect against GC-induced osteoporosis in rats.https://www.frontiersin.org/articles/10.3389/fendo.2022.932488/fullosteoporosisdieckolhormoneantioxidantinflammationbone turnover parameter
spellingShingle Hao Wang
Leigang Yang
Junwei Chao
Antiosteoporosis and bone protective effect of dieckol against glucocorticoid-induced osteoporosis in rats
Frontiers in Endocrinology
osteoporosis
dieckol
hormone
antioxidant
inflammation
bone turnover parameter
title Antiosteoporosis and bone protective effect of dieckol against glucocorticoid-induced osteoporosis in rats
title_full Antiosteoporosis and bone protective effect of dieckol against glucocorticoid-induced osteoporosis in rats
title_fullStr Antiosteoporosis and bone protective effect of dieckol against glucocorticoid-induced osteoporosis in rats
title_full_unstemmed Antiosteoporosis and bone protective effect of dieckol against glucocorticoid-induced osteoporosis in rats
title_short Antiosteoporosis and bone protective effect of dieckol against glucocorticoid-induced osteoporosis in rats
title_sort antiosteoporosis and bone protective effect of dieckol against glucocorticoid induced osteoporosis in rats
topic osteoporosis
dieckol
hormone
antioxidant
inflammation
bone turnover parameter
url https://www.frontiersin.org/articles/10.3389/fendo.2022.932488/full
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