The mechanism of Epimedin B in treating osteoporosis as revealed by RNA sequencing‐based analysis

Abstract

With the ageing of populations, the management of osteoporosis is a priority of society in general. Epimedin B, a major ingredient of Herba Epimedii, which has the advantages of high content and hypotoxicity has been proved to be effective in preventing osteoporosis in vitro. However, the efficacy and mechanism of Epimedin B on osteoporosis in vivo have not been well elucidated yet. This study aimed to investigate the effects and the potential mechanisms of 8-week repeated oral administration of Epimedin B (10 and 20 mg/ kg/day) on a mouse osteoporosis model. Effects of Epimedin B were evaluated by examinations of serum bone turnover markers, bone mineral density, bone microstructure parameters and histopathological section. Epimedin B significantly rose N-terminal propeptide of type I procollagen (P1NP) and dropped C-telopeptide of type I collagen (CTX1). Connectivity density (Conn.D) increased significantly while structure model index (DA) decreased significantly after treated by Epimedin B. Meanwhile, Epimedin B administration significantly increased the number of trabecular bones while significantly decreased the gap between them. Overall, Epimedin B showed beneficial effects on osteoporosis. Furthermore, RNA sequencing-based analysis revealed 5 significantly down-regulated transcripts and 107 significantly up-regulated transcripts between the Epimedin B administration group and the model group. These transcripts were mapped to 15 pathways by KEGG enrichment analysis, of which PI3K-Akt signalling pathway, MAPK signalling pathway and PPAR signalling pathway were most connected to osteoporosis. To conclude, Epimedin B is effective in treating osteoporosis in mice via regulating PI3K-Akt, MAPK and PPAR signalling pathway.

Epimedin B exhibits pigmentation by increasing tyrosinase family proteins expression, activity, and stability

“…Thus far, only a few bioactivity or pharmacological studies on EB are available, and these studies describe the function of EB in osteoporosis treatment, nerve protection, and immune activity stimulation [ [20] , [21] , [22] ]. In this study, we provided comprehensive evidence of EB function in pigmentation in vivo and in vitro , using melanoma cells, human primary melanocytes, human skin-organ explant culture, and depigmented zebrafish and C57BL/6 mice; we also elucidated the multiple mechanisms regulating melanogenesis by increasing TYR expression, activity, and stability.…”

Epimedium‐Curculigo herb pair enhances bone repair with infected bone defects and regulates osteoblasts through LncRNA MALAT1/miR‐34a‐5p/SMAD2 axis

“… 35 , 36 , 37 Meanwhile, Baohuoside I is one of the metabolites of Icariin in vivo and also one of the main active flavonoid components of the Epimedium brevicornum maxim . 38 Previous studies have shown that Curculigoside, the effective substance of Curculigo orchioides, could attenuate wear particle‐induced periprosthetic osteolysis by promoting osteoblastic MC3T3‐E1 cell differentiation and inhibiting osteoclast BMSC formation. 39 It is important to note that there is currently a lack of literature on the correlation between Orcinol glucoside and bone.…”

Chinese Proprietary Medicine Xianling Gubao Capsule for Osteoporosis: A Systematic Review and Meta-Analysis of Randomized Clinical Trials

“…Sweroside interacts with membrane estrogen receptor-α and p38 pathway to promote osteoblastic differentiation and mineralization ( 35 ). Epimedin B downregulates PI3K-Akt, MAPK, and PPAR signaling pathways, which are mentioned above to result in bone destruction in mice ( 36 ) and have estrogen-like effects ( 37 ). Some other compounds like isopsoralen, asperosaponin VI, and neobavaisoflavone have also been proved to either enhance osteogenesis or inhibit osteoclast activation ( 38 – 42 ).…”