| First Author | Hoshi H | Year | 2020 |
| Journal | Biochem Biophys Res Commun | Volume | 527 |
| Issue | 1 | Pages | 270-275 |
| PubMed ID | 32446379 | Mgi Jnum | J:310625 |
| Mgi Id | MGI:6713399 | Doi | 10.1016/j.bbrc.2020.04.013 |
| Citation | Hoshi H, et al. (2020) Astaxanthin improves osteopenia caused by aldehyde-stress resulting from Aldh2 mutation due to impaired osteoblastogenesis. Biochem Biophys Res Commun 527(1):270-275 |
| abstractText | Aldehyde dehydrogenase 2 (ALDH2) plays major roles in aldehyde detoxification and in the catalysis of amino acids. ALDH2 *2, a dominant-negative transgenic expressing aldehyde dehydrogenase 2 (ALDH2) protein, is produced by a single nucleotide polymorphism (rs671) and is involved in the development of osteoporosis and hip fracture with aging. In a previous study, transgenic mice expressing Aldh2 *2(Aldh2 *2 Tg) osteoblastic cells or acetaldehyde -treated MC3T3-E1 showed impaired osteoblastogenesis and caused osteoporosis [1]. In this study, we demonstrated the effects of astaxanthin for differentiation to osteoblasts of MC3T3-E1 by the addition of acetaldehyde and Aldh2 *2 Tg mesenchymal stem cells in bone marrow. Astaxanthin restores the inhibited osteoblastogenesis by acetaldehyde in MC 3T3-E1 and in bone marrow mesenchymal stem cells of Aldh2 *2 Tg mice. Additionally, astaxanthin administration improved femur bone density in Aldh2 *2 Tg mice. Furthermore, astaxanthin improved cell survival and mitochondrial function in acetaldehyde-treated MC 3T3-E1 cells. Our results suggested that astaxanthin had restorative effects on osteoblast formation and provide new insight into the regulation of osteoporosis and suggest a novel strategy to promote bone formation in osteopenic diseases caused by impaired acetaldehyde metabolism. |
