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

Abstract

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.

Agomelatine alleviates steroid‐induced osteoporosis by targeting SIRT1/RANKL/FOXO1/OPG signalling in rats

“…The level of RANKL's receptor and the existence of OPG, which prohibit RANKL binding to RANK, determine the cellular response to RANKL. 47 In this context, Wang et al 48 showed that dexamethasone injected in a dose of (2.5 mg/kg/day) for 5 days caused elevation in osteocalcin and TRACP levels, reduction of OPG level with an elevation of RANKL plasma level as confirmed in our results.…”

“…The level of RANKL's receptor and the existence of OPG, which prohibit RANKL binding to RANK, determine the cellular response to RANKL 47 . In this context, Wang et al 48 showed that dexamethasone injected in a dose of (2.5 mg/kg/day) for 5 days caused elevation in osteocalcin and TRACP levels, reduction of OPG level with an elevation of RANKL plasma level as confirmed in our results. Moreover, Bastawy et al 49 stated that prednisolone, given daily for 2 months, at a dose level of (4.05 mg/kg), caused elevated levels of ALP and TRACP with decreased immunohistochemical expression of OPG, the bone‐forming indicator and increased RANKL expression, and this was linked to prednisolone‐induced osteoporosis.…”

“…The aetiology of bone loss seems to be complicated by changes in ROS and/or antioxidant systems. 50 In this context, Wang et al 48 showed that there was an T A B L E 7 Comparing collagen area % in the studied groups. Finding the potential molecular processes that would explain agomelatine's effects on steroid-induced osteoporosis was crucial.…”

Tricrilactones A–H, Potent Antiosteoporosis Macrolides with Distinctive Ring Skeletons fromTrichocladium crispatum, an Alpine Moss‐Associated Fungus

“…bisphosphonates and denosumab). [5] Nevertheless, most of the targeted therapies have limitations due to their serious adverse effects, such as stroke, musculoskeletal pain, nausea, hypercalcemia, and so forth. [2,5] Therefore, exploring a new generation of antiosteoporosis drugs with high efficacy but few side effects remains an urgent need.…”

“…Current strategies for osteoporosis therapy include calcium administration, vitamin supplement, and estrogen receptor modulation, as well as medical treatments (e.g. bisphosphonates and denosumab) [5] . Nevertheless, most of the targeted therapies have limitations due to their serious adverse effects, such as stroke, musculoskeletal pain, nausea, hypercalcemia, and so forth [2, 5] .…”