Abstract
Osteoporosis is characterized by a reduction of the bone mineral density (BMD) and microarchitectural deterioration of the bone, which lead to bone fragility and susceptibility to fracture. Astaxanthin (AST) has a variety of biological activities, such as a protective effect against asthma or neuroinflammation, antioxidant effect, and decrease of the osteoclast number in the right mandibles in the periodontitis model. Although treatment with AST is known to have an effect on inflammation, no studies on the effect of AST exposure on bone loss have been performed. Thus, in the present study, we examined the antiosteoporotic effect of AST on bone mass in ovariectomized (OVX) mice and its possible mechanism of action. The administration of AST (5, 10 mg/kg) for 6 weeks suppressed the enhancement of serum calcium, inorganic phosphorus, alkaline phosphatase, total cholesterol, and tartrate-resistant acid phosphatase (TRAP) activity. The bone mineral density (BMD) and bone microarchitecture of the trabecular bone in the tibia and femur were recovered by AST exposure. Moreover, in the in vitro experiment, we demonstrated that AST inhibits osteoclast formation through the expression of the nuclear factor of activated T cells (NFAT) c1, dendritic cell-specific transmembrane protein (DC-STAMP), TRAP, and cathepsin K without any cytotoxic effects on bone marrow-derived macrophages (BMMs). Therefore, we suggest that AST may have therapeutic potential for the treatment of postmenopausal osteoporosis.
Highlights
Osteoporosis has been widely recognized as a major health issue and is a skeletal disease characterized by the reduction of bone mass and deterioration of the microarchitecture in bone tissue with a consequent increase in bone fragility [1]
In order to evaluate the effect of AST (Figure 1A) on osteoclast differentiation, we added AST during osteoclast differentiation with receptor activators of nuclear factor kappa-B ligand (RANKL) and macrophage colony stimulating factor (M-CSF)
An estimated ten million Americans have osteoporosis, and over 1.5 million fractures per year are attributed to osteoporosis, including approximately 300,000 hip fractures
Summary
Osteoporosis has been widely recognized as a major health issue and is a skeletal disease characterized by the reduction of bone mass and deterioration of the microarchitecture in bone tissue with a consequent increase in bone fragility [1]. RANKL is expressed on the osteoblast cells and induces the essential signal for precursor cells to differentiate into osteoclasts. The binding of RANKL to its receptor RANK in bone marrow-derived monocyte/macrophage precursor cells (BMMs) results in the recruitment of TNF receptor-associated factor 6 (TRAF 6), which is linked to the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and the Jun N-terminal kinase (JNK) pathway [7]. The ideal treatment strategy for osteoporosis is to inhibit bone resorption by osteoclasts and/or increase bone formation by osteoblasts. The effect of astaxanthin on osteoclast differentiation and bone loss in osteoporosis animal models has not been studied yet. We demonstrated the inhibitory effects of astaxanthin on osteoclast differentiation and trabecular bone loss
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