Abstract
We explored how tabersonine (Tab) protected against dexamethasone (Dex)-induced osteoporosis. Osteoblasts were treated with Dex (100 µM) with or without Table (5 or 10 µM). We measured cell viability, alkaline phosphatase (ALP) activity, and mitochondrialsuperoxide and reactive oxygen species levels. We used flow cytometry to explore the effects of Tab on mitochondrial membrane potential and osteoblast apoptosis. We used RT-PCR and western blotting to examine the effect of Tab on protein expression. We evaluated the effects of Tab on bone histopathology and bone mineral density in rats with Dex-induced osteoporosis. Tab increased cell viability and ALP activity, and reduced the mitochondrial superoxide, reactive oxygen species and matrix metalloproteinase levels and osteoblast apoptosis. Tab significantly reduced the levels of nuclear factor erythroid 2-related factor 2 (Nrf2), haem oxygenase-1 and NAD(P)H quinone dehydrogenase 1. Moreover, it increased the levels of mRNAs encoding runt-related transcription factor 2, bone morphogenetic protein-2 and osterix. These data suggest that Tab ameliorates Dex-induced osteoporosis by regulating the Nrf2 signalling pathway.
Highlights
Osteoporosis is a metabolic bone disease characterised by the loss of bone mass and bone weakness; it affects about 200 million individuals (80% of whom are female) worldwide (Sözen et al 2017)
Effect of Tab on alkaline phosphatase (ALP) activity Dex significantly reduced the osteoblast ALP level compared with the control (p < 0.01; Fig. 2), and Tab neutralised this negative effect of Dex
Bone homeostasis is affected by osteoporosis, a disease characterised by the dysregulation of bone formation and resorption
Summary
Osteoporosis is a metabolic bone disease characterised by the loss of bone mass and bone weakness; it affects about 200 million individuals (80% of whom are female) worldwide (Sözen et al 2017). Skeletal integrity is compromised in osteoporotic patients; an imbalance develops between bone formation and resorption, triggering fracture (Office of the Surgeon General (USA) 2004). Osteoblasts are responsible for bone formation and mineralisation. Oestrogen enhances osteoblastic mineralisation and stimulates osteoblast differentiation and proliferation (Domazetovic et al 2017).
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
