Raloxifene in the Treatment of Osteoporosis in Postmenopausal Women
                    with End-Stage Renal Disease: A Systematic Review and
                    Meta-Analysis

Ma, Haoyang; Chen, Shuang; Lu, Lingling; Gong, Wenbin; Zhang, Aihua

doi:10.1055/a-1655-4362

Cited by 11 publications

(1 citation statement)

References 51 publications

(68 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…2,3 Furthermore, antibone resorption drugs include calcitonin, bisphosphonates, selective oestrogen receptor modulators, Cathepsin K (CTSK) inhibitor and specific RANKL monoclonal antibodies. The representative antiosteoporosis drugs include salmon calcitonin, 4 zoledronate sodium, 5 raloxifene, 6 denosumab. 7 Currently, anti-osteoporosis regimens mainly depend on the administration of calcium, vitamin D and anti-osteoporosis drugs.…”

Section: Introductionmentioning

confidence: 99%

Myricitrin promotes osteogenesis and prevents ovariectomy bone mass loss via the PI3K/AKT signalling pathway

Mai

Zhang

et al. 2023

J of Cellular Biochemistry

View full text Add to dashboard Cite

This study aimed to explore the effect of myricitrin on osteoblast differentiation in mice immortalised bone marrow mesenchymal stem cells (imBMSCs). Additionally, ovariectomy (OVX) mice were employed to examine the effect of myricitrin on bone trabecular loss in vivo. The effect of myricitrin on the proliferation of imBMSCs was evaluated using a cell counting kit‐8 assay. Alizarin red staining, alkaline phosphatase staining were performed to elucidate osteogenesis. Furthermore, qRT‐PCR and western blot determined the expression of osteo‐specific genes and proteins. To screen for candidate targets, mRNA transcriptome genes were sequenced using bioinformatics analyses. Western blot and molecular docking analysis were used to examine target signalling markers. Moreover, rescue experiments were used to confirm the effect of myricitrin on the osteogenic differentiation of imBMSCs. OVX mice were also used to estimate the delay capability of myricitrin on bone trabecular loss in vivo using western blot, micro‐CT, tartaric acid phosphatase (Trap) staining, haematoxylin and eosin staining, Masson staining and immunochemistry. In vitro, myricitrin significantly enhanced osteo‐specific genes and protein expression and calcium deposition. Moreover, mRNA transcriptome gene sequencing and molecular docking analysis revealed that this enhancement was accompanied by an upregulation of the PI3K/AKT signalling pathway. Furthermore, copanlisib, a PI3K inhibitor, partially reversed the osteogenesis promotion induced by myricitrin. In vivo, western blot, micro‐CT, hematoxylin and eosin staining, Masson staining, Trap staining and immunochemistry revealed that bone trabecular loss rate was significantly alleviated in the myricitrin low‐ and high‐dose groups, with an increased expression of osteopontin, osteoprotegerin, p‐PI3K and p‐AKT compared to the OVX group. Myricitrin enhances imBMSC osteoblast differentiation and attenuate bone mass loss partly through the upregulation of the PI3K/AKT signalling pathway. Thus, myricitrin has therapeutic potential as an antiosteoporosis drug.

show abstract