4.7 Article

Structural identification of an polysaccharide isolated from Epimedium brevicornum and its beneficial effect on promoting osteogenesis in osteoblasts induced by high glucose

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BIOMEDICINE & PHARMACOTHERAPY
卷 169, 期 -, 页码 -

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ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2023.115893

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Diabetes osteoporosis; Epimedium brevicornum polysaccharide; Structural resolution; Pharmacological mechanisms

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The main component of Epimedium brevicornum, EBPC1, was found to promote osteogenesis during diabetes osteoporosis and inhibit apoptosis by regulating Bax/Bcl2. This study reveals the potential application of Epimedium brevicornum in the treatment of bone diseases.
Aim: Diabetes osteoporosis (DOP) is a chronic bone metabolic disease induced by diabetes, whose morbidity continues to increase. Epimedium brevicornum Maxim (EB), a popular Chinese traditional medicine, has been used to treat bone diseases in China for thousands of years. But its material basis and specific mechanism of action are not clear. Methods: Epimedium brevicornum crude polysaccharide (EPE) is the main component, in this research the characterized the structure of EBPC1 purified from EPE was detected and its effects on cell proliferation, differentiation, and cytoskeletal in osteoblasts induced by high glucose. Results: The molecular weight of EBPC1 was 10.5 kDa. It was mainly comprised of glucose and galactose, and the backbone of EBPC1 was -> 4)-alpha-D-Galp-(1 -> 4)-alpha-D-Galp-(1 -> 6)-beta-D-Galp-(1 -> 6)-beta-D-Galp-(1 -> 4)-alpha-D-Glcp-(1 -> 4)alpha-D-Glcp-(1 ->. The results from in vitro experiments revealed that EBPC1 significantly increased alkaline phosphatase (ALP) activity and mineralized nodule formation in primary osteoblasts, also significantly upregulated expression of Alp mRNA and Runx2 mRNA in the presence of EBPC1 pretreatment. Moreover, EBPC1 modulated apoptosis via the regulation of Bax/Bcl2. Conclusion: These results indicate that EBPC1 treatment can promote osteogenesis during DOP, which can ameliorate apoptosis by regulating Bax/Bcl2 and accelerating osteogenesis in osteoblasts.

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