2. Academic Validation
  3. The Role of Rosavin in the Pathophysiology of Bone Metabolism

The Role of Rosavin in the Pathophysiology of Bone Metabolism

  • Int J Mol Sci. 2024 Feb 9;25(4):2117. doi: 10.3390/ijms25042117.
Piotr Wojdasiewicz 1,  Paweł Turczyn 2,  Anna Lach-Gruba 3,  Łukasz A Poniatowski 4,  Daryush Purrahman 5,  Mohammad-Reza Mahmoudian-Sani 5,  Dariusz Szukiewicz 1
Affiliations

Affiliations

  • 1 Department of Biophysics, Physiology and Pathophysiology, Faculty of Health Sciences, Medical University of Warsaw, Chałubińskiego 5, 02-004 Warsaw, Poland.
  • 2 Department of Early Arthritis, Eleonora Reicher National Institute of Geriatrics, Rheumatology and Rehabilitation, Spartańska 1, 02-637 Warsaw, Poland.
  • 3 Department of Rehabilitation, St. Anna's Trauma Surgery Hospital, Mazovian Rehabilitation Center-STOCER, Barska 16/20, 02-315 Warsaw, Poland.
  • 4 Department of Neurosurgery, Dietrich-Bonhoeffer-Klinikum, Salvador-Allende-Straße 30, 17036 Neubrandenburg, Germany.
  • 5 Thalassemia and Hemoglobinopathy Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
PMID: 38396794 DOI: 10.3390/ijms25042117
Abstract

Rosavin, a phenylpropanoid in Rhodiola rosea's rhizome, and an adaptogen, is known for enhancing the body's response to environmental stress. It significantly affects cellular metabolism in health and many diseases, particularly influencing bone tissue metabolism. In vitro, rosavin inhibits osteoclastogenesis, disrupts F-actin ring formation, and reduces the expression of osteoclastogenesis-related genes such as Cathepsin K, Calcitonin receptor (CTR), tumor necrosis factor receptor-associated factor 6 (TRAF6), tartrate-resistant Acid Phosphatase (TRAP), and matrix metallopeptidase 9 (MMP-9). It also impedes the nuclear factor of activated T-cell cytoplasmic 1 (NFATc1), c-Fos, the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and mitogen-activated protein kinase (MAPK) signaling pathways and blocks phosphorylation processes crucial for bone resorption. Moreover, rosavin promotes osteogenesis and osteoblast differentiation and increases mouse runt-related transcription factor 2 (Runx2) and osteocalcin (OCN) expression. In vivo studies show its effectiveness in enhancing bone mineral density (BMD) in postmenopausal osteoporosis (PMOP) mice, restraining osteoclast maturation, and increasing the active osteoblast percentage in bone tissue. It modulates mRNA expressions by increasing eukaryotic translation elongation factor 2 (EEF2) and decreasing histone deacetylase 1 (HDAC1), thereby activating osteoprotective epigenetic mechanisms, and alters many serum markers, including decreasing cross-linked C-telopeptide of type I collagen (CTX-1), tartrate-resistant Acid Phosphatase 5b (TRACP5b), receptor activator for nuclear factor κ B ligand (RANKL), macrophage-colony-stimulating factor (M-CSF), and TRAP, while increasing Alkaline Phosphatase (ALP) and OCN. Additionally, when combined with zinc and probiotics, it reduces pro-osteoporotic matrix metallopeptidase 3 (MMP-3), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α), and enhances anti-osteoporotic interleukin 10 (IL-10) and tissue inhibitor of metalloproteinase 3 (TIMP3) expressions. This paper aims to systematically review rosavin's impact on bone tissue metabolism, exploring its potential in osteoporosis prevention and treatment, and suggesting future research directions.

Keywords

Rhodiola rosea; adaptogens; bone loss; bone metabolism; osteoblasts; osteoclastogenesis; osteogenesis; osteoporosis; rosavin.

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