Daphnetin ameliorates glucocorticoid-induced osteoporosis via activation of Wnt/GSK-3β/β-catenin signaling

Wang, Yongkui; Chen, Jian; Chen, Jing; Dong, Chao; Xu, Yan; Zhu, Zhongpei; Lü, Ping; Song, Zongmian; Liu, Hongjian; Chen, Songfeng

doi:10.1016/j.taap.2020.115333

Cited by 22 publications

(23 citation statements)

References 45 publications

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“…The calcium and Currently, most treatments in clinic for osteoporosis are phosphate supplements or targeting through regulating bone metabolism by RANKL/OPG pathway (Compston et al, 2019). MAPK/NF-κB and Wnt/GSK-3β/β-catenin signaling pathway are also demonstrated to play important roles in osteoclast genesis Wang et al, 2020). Xiao L. et al found Puerarin can suppress osteoclastogenesis via inhibition of TRAF6/ROSdependent MAPK/NF-κB signaling pathways (Masanobu, 2014) Finally, our experiment also has limitations.…”

Section: Discussionmentioning

confidence: 99%

Eucommia, Cuscuta, and Drynaria Extracts Ameliorate Glucocorticoid-Induced Osteoporosis by Inhibiting Osteoclastogenesis Through PI3K/Akt Pathway

Han

Li²,

Zhang

et al. 2022

Front. Pharmacol.

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Osteoporosis is one of the most common diseases in the world which resulted in heavy socioeconomic burden and a public health threat. Glucocorticoid-induced osteoporosis (GIO) is the most common secondary reason of osteoporosis. Therapeutic strategies using traditional Chinese medicine are under investigation for osteoporosis, with efforts to improve efficacy and clarify the mechanism. The combination of Eucommia, Cuscuta, and Drynaria is widely used in traditional Chinese decoction for osteoporosis treatment, but the experimental efficacy and mechanism are still unclear. Administration of E.C.D. extracts (Eucommia, Cuscuta, and Drynaria) in experimental GIO rats resulted in decreased urinal calcium, phosphorus loss, and decreased expression of RANKL, CTX in serum, increased serum calcium, phosphorus, and OPG level. E.C.D. extracts also improved bone density, structural integrity, and biomechanical function in experimental GIO rats. These finding were associated with E.C.D. extracts’ treatment efficacy to GIO in vivo. The balance between osteoclast and osteoblast activity is essential for bone remodeling and bone related disease. The E.C.D. extracts inhibited Raw 264.7 cell differentiation to osteoclast in vitro. On the other hand, it promoted OPG expression of bone marrow mesenchymal stromal cells (MSCs) which can suppress the osteoclast genesis. E.C.D. extracts also increased the Wnt1 and Runx2 expression which are related to osteoblast formation. It also regulated the paracrine effect of MSC to inhibit osteoclast differentiation. The analysis of HPLC and comprehensive pharmacology identified the constituents of E.C.D. extracts and the potential osteoporosis-related targets mediated by E.C.D. extracts. The KEGG enrichment analysis suggested that PI3K/Akt pathway may be involved in the regulation osteoclast genesis by E.C.D. extracts and the result of Western blot of vitro assays proved it. Collectively, these data demonstrate E.C.D. extracts can inhibit osteoclast differentiation to foster experimental osteoporosis both in vivo and in vitro and it may exert the function of inhibiting osteoclast differentiation through PI3K/Akt pathway.

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Section: Discussionmentioning

confidence: 99%

Eucommia, Cuscuta, and Drynaria Extracts Ameliorate Glucocorticoid-Induced Osteoporosis by Inhibiting Osteoclastogenesis Through PI3K/Akt Pathway

Han

Li²,

Zhang

et al. 2022

Front. Pharmacol.

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“…Aberrant Wnt/β-catenin signaling can lead to osteopenic states and skeletal disorders [13,16]. GC was found to produce severe alterations in Wnt/βcatenin pathway, disrupting the balance between osteoblastogenesis and adipogenesis of MSCs [13,17]. In contrast, the non-canonical Wnt proteins, Wnt5a, bind to the receptor complex of Fz and the receptor tyrosine kinase-like orphan receptors (Rors) 1/2 as co-receptors activating Wnt/Ca 2+ pathways and Wnt/planar cell polarity pathways [18,19].…”

Section: Introductionmentioning

confidence: 99%

Phoenix dactilyfera L. Pits Extract Restored Bone Homeostasis in Glucocorticoid-Induced Osteoporotic Animal Model through the Antioxidant Effect and Wnt5a Non-Canonical Signaling

et al. 2022

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Oxidative stress associated with long-term glucocorticoids administration is a route through which secondary osteoporosis can be developed. The therapeutic potential of Phoenix dactilyfera L. pits is offered by their balanced, valuable and diverse phytochemical composition providing protective potential against oxidative reactions, making it a good candidate to treat glucocorticoid-induced osteoporosis (GIO). This study evaluates the possible anti-osteoporotic effect of date pit extract (DPE) against dexamethasone (DEXA)-induced osteoporosis. Male rats were allocated into three control groups, which received saline, low and high doses of DPE (150 and 300 mg/kg/day), respectively. Osteoporosis-induced groups that received DEXA (1 mg/kg/day) were divided into DEXA only, DPE (2 doses) + DEXA, and ipriflavone + DEXA. Femoral bone minerals density and bone mineral content, bone oxidative stress markers, Wnt signaling, osteoblast and osteoclast differentiation markers, and femur histopathology were evaluated. DPE defeated the oxidative stress, resulting in ameliorative changes in Wnt signaling. DPE significantly reduced the adipogenicity and abolished the osteoclastogenic markers (RANKL/OPG ratio, ACP, TRAP) while enhancing the osteogenic differentiation markers (Runx2, Osx, COL1A1, OCN). In Conclusion DPE restored the balanced proliferation and differentiation of osteoclasts and osteoblasts precursors. DPE can be considered a promising remedy for GIO, especially at a low dose that had more potency.

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“…It has been well accepted that there is a strong correlation between long-term glucocorticoids therapy and the development of osteoporosis ( Ding et al, 2015 ; Liu et al, 2018 ). Growing evidence from in vitro and in vivo studies shows that glucocorticoids can inhibit osteoblast proliferation and promote its apoptosis, subsequently resulting in the suppression of bone production and growth ( Wang Y. et al, 2020 ; Wang L. et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Hesperidin Ameliorates Dexamethasone-Induced Osteoporosis by Inhibiting p53

Zhang

Chen

Zeng

et al. 2022

Front. Cell Dev. Biol.

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Osteoporosis is one of the most frequent skeletal disorders and a major cause of morbidity and mortality in the expanding aging population. Evidence suggests that hesperidin may have a therapeutic impact on osteoporosis. Nevertheless, little is known about the role of hesperidin in the development of osteoporosis. Bioinformatics analyses were carried out to explore the functions and possible molecular mechanisms by which hesperidin regulates osteogenic differentiation. In the present study, we screened and harvested 12 KEGG pathways that were shared by hesperidin-targeted genes and osteoporosis. The p53 signaling pathway was considered to be a key mechanism. Our in vitro results showed that hesperidin partially reversed dexamethasone-induced inhibition of osteogenic differentiation by suppressing the activation of p53, and suggest that hesperidin may be a promising candidate for the treatment against dexamethasone-induced osteoporosis.

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Daphnetin ameliorates glucocorticoid-induced osteoporosis via activation of Wnt/GSK-3β/β-catenin signaling

Cited by 22 publications

References 45 publications

Eucommia, Cuscuta, and Drynaria Extracts Ameliorate Glucocorticoid-Induced Osteoporosis by Inhibiting Osteoclastogenesis Through PI3K/Akt Pathway

Eucommia, Cuscuta, and Drynaria Extracts Ameliorate Glucocorticoid-Induced Osteoporosis by Inhibiting Osteoclastogenesis Through PI3K/Akt Pathway

Phoenix dactilyfera L. Pits Extract Restored Bone Homeostasis in Glucocorticoid-Induced Osteoporotic Animal Model through the Antioxidant Effect and Wnt5a Non-Canonical Signaling

Hesperidin Ameliorates Dexamethasone-Induced Osteoporosis by Inhibiting p53

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