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In Vitro Cellular and Developmental Biology - Animal 2018-May

In vitro evaluation of the potential therapeutic role of Dendropanax morbifera extract in ameliorating osteoporosis and resultant bone impairment using MC3T3-E1 cells.

يمكن للمستخدمين المسجلين فقط ترجمة المقالات
الدخول التسجيل فى الموقع
يتم حفظ الارتباط في الحافظة
Dong-Uk Yang
Muhammad Hanif Siddiqi
Sungeun Ahn
Sera Kang
Hae-Yong Noh
Deok-Chun Yang

الكلمات الدالة

نبذة مختصرة

Osteoporosis is a widespread musculoskeletal deformity that affects thousands of older people every year, leading to bone abnormalities and ultimately increasing the risk of bone fractures in both genders. It is considered a lethal disease causing death in thousands of people at the late stage of life. Dendropanax morbifera Leveille is a subtropical broad-leaved prevalent species in Korea. Extracts of the leaves, stems, roots, and seeds of D. morbifera have been used in traditional medicine for the treatment of numerous diseases such as diabetes, atherogenesis, skin disorders, and headaches. However, the anti-osteoporosis effects of D. morbifera have not been examined. The primary objectives of this study were to elucidate the anti-osteoporosis effect of D. morbifera extract through an in vitro study using pre-osteoblastic MC3T3-E1 cells. We found that D. morbifera strongly increased the expression of bone metabolic markers such as alkaline phosphatase (ALP) activity, type I collagen (Col-I) level, and mineralization. Additionally, D. morbifera extract also upregulated the mRNA expression levels of osteogenic genes including ALP, osteocalcin (OCN), osterix (Osx), and runt-related transcription factor 2 (Runx2) in MC3T3-E1 cells via upregulation of bone morphogenetic protein 2 (BMP-2)/p38 MAPK/JNK and Smad1/5/8 signaling pathways. Moreover, addition of D. morbifera significantly suppressed the inhibitory effect of SB203580 (p38 inhibitor). In conclusion, the current study demonstrated that D. morbifera extract significantly increased osteoblast differentiation and mineralization in MC3T3-E1 cells by regulating BMP-2/p38/JNK and Smad1/5/8. Our study might be helpful in the discovery and development of new anti-osteoporosis therapeutic agents.

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