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- 저자 : ( Mahesh Sapkota ) (검색결과 2 건)
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( Mahesh Sapkota ),( Liang Li ),( Hyukjae Choi ),( William H Gerwick ),( Yunjo Soh ) 영남대학교 약품개발연구소 2016 영남대학교 약품개발연구소 연구업적집 Vol.26 No.-
Osteoclasts are unique bone remodeling cells derived from multinucleated myeloid progenitor cells. They play homeostatic vital roles in skeletal modeling and remodeling but also destroy bone masses in many pathological conditions such as osteoporosis and rheumatoid arthritis. Receptor activation of NF-KB li-gand (RANKL) is essential osteclastogenesis. In this study, we investigated the effects of bromo-honaucin A (Br-H A) isolated from Leptolyngbya crossbyana (cyanobacterium). To investigate the me-chanism of the inhibitory effect of Br-H A on osteoclstogenesis. we employed Br-H Ain RANKL-treated murine monocyte/macrophage RAW 264.7 cells for osteoclastic differentiation in-vitro. The inhibitory effects on in-vitro osteoclastogenesis was evaluated by counting the number of Tartarate resistant acid phospatase (TRAP) positive multinucleated cells and by measuring the expression level of osteoclast-specific genes like matrix metalloproteinase 9 (MMP9). cathepsin K (CATH K), GRB2-associated-binding protein 2 (GAB2), c-terminal myc kinase (C-MYC). C-terminal Src kinase (C-SRC) and Microphthalmia-associated transcription factor (MITF). Moreover, Br-H A blocked the resorbing capacity of RAW 264.7 cells on calcium phosphate-coated plates. Finally, Br-H A clearly decreased the expression of Akt and also decreased the activation of ERK. Thus, the study identifies Br-H A as potent inhibitor potentialin the treatment of diseases involving abnormal bone lysis such as osteoporosis. rheumatoid arthritis, and periodontal bone degradation.
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Sapkota, Mahesh,Shrestha, Saroj Kumar,Yang, Ming,Park, Young Ran,Soh, Yunjo Elsevier 2019 european journal of pharmacology Vol.865 No.-
<P><B>Abstract</B></P> <P>Vascular calcification increases the risk of morbidity and mortality in patients with cardiovascular diseases, chronic kidney diseases, and diabetes. However, viable therapeutic methods to target vascular calcification are limited. Aloe-emodin (AE), an anthraquinone is a natural compound found in the leaves of Aloe-vera. In this study, we investigated the underlying mechanism of AE in the calcification of vascular smooth muscle cells (VSMCs) and murine thoracic aorta. We demonstrate that AE repressed not only the phenotypes of Ca<SUP>2+</SUP> induced calcification but also level of calcium in VSMCs. AE has no effect on cell viability in VSMC cells. Alizarin red, von Kossa stainings and calcium quantification showed that Ca<SUP>2+</SUP> induced vascular calcification is significantly decreased by AE in a concentration-dependent manner. In contrast, AE attenuated Ca<SUP>2+</SUP> induced calcification through inhibiting osteoblast differentiation genes such as SMAD4, collagen 1α, osteopontin (OPN), Runt-related transcription factor (RUNX-2) and Osterix. AE also suppressed Ca<SUP>2+</SUP> induced osteoblast-related protein expression including collagen 1α, bone morphogenic protein 2 (BMP-2), RUNX-2 and smooth muscle actin (SMA). Furthermore, Alizarin red, von Kossa stainings and calcium quantification showed that AE significantly inhibited the calcification of <I>ex vivo</I> ring formation in murine thoracic aorta, and markedly inhibited vitamin D<SUB>3</SUB> induced medial aorta calcification <I>in vivo</I>. Taken together, our findings suggest that AE may have therapeutic potential for the prevention of vascular calcification program.</P>
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