Abstract Title:

Astaxanthin improves osteopenia caused by aldehyde-stress resulting from Aldh2 mutation due to impaired osteoblastogenesis.

Abstract Source:

Biochem Biophys Res Commun. 2020 Jun 18 ;527(1):270-275. Epub 2020 May 4. PMID: 32446379

Abstract Author(s):

Hiroko Hoshi, Fuka Monoe, Ikuroh Ohsawa, Shigeo Ohta, Takeshi Miyamoto

Article Affiliation:

Hiroko Hoshi


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 byimpaired acetaldehyde metabolism.

Study Type : Animal Study

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