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Suppression Effect of Astaxanthin on Osteoclast Formation In Vitro and Bone Loss In Vivo

Hwang, Yun-Ho, Kim, Kwang-Jin, Kim, Su-Jin, Mun, Seul-Ki, Hong, Seong-Gyeol, Son, Young-Jin, Yee, Sung-Tae·2018·International Journal of Molecular Sciences
DOI 10.3390/ijms19030912PMC PMC5877773
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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.

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Figures

Figure 1 Astaxanthin suppresses osteoclastogenesis. (A) Chemical structure of Astaxanthin; (B) BMMs prepared from bone marrow cells were cultured for 4 days with RANKL (10 ng/mL) and M-CSF (30 ng/mL) in the presence of the indicated concentrations of Astaxanthin or 0.1% DMSO (control vehicle). The cells were fixed in 3.7% formalin, permeabilized in 0.1% Triton X-100, and stained for TRAP, a marker enzyme of osteoclasts; (C) TRAP-positive multinuclear cells (nuclei ≥ 3) were counted as osteoclasts. * p <0.05, ** p < 0.01, *** p <0.001; (D) The effect of Astaxanthin on the viability of BMMs was evaluated by CCK-8 assay. In (C, D), n = 3.
Figure 1 Astaxanthin suppresses osteoclastogenesis. (A) Chemical structure of Astaxanthin; (B) BMMs prepared from bone marrow cells were cultured for 4 days with RANKL (10 ng/mL) and M-CSF (30 ng/mL) in the presence of the indicated concentrations of Astaxanthin or 0.1% DMSO (control vehicle). The cells were fixed in 3.7% formalin, permeabilized in 0.1% Triton X-100, and stained for TRAP, a marker enzyme of osteoclasts; (C) TRAP-positive multinuclear cells (nuclei ≥ 3) were counted as osteoclasts. * p <0.05, ** p < 0.01, *** p <0.001; (D) The effect of Astaxanthin on the viability of BMMs was evaluated by CCK-8 assay. In (C, D), n = 3.CC BY · PubMed Central
Figure 2 Astaxanthin inhibits the expression of the genes involved in osteoclastogenesis. BMMs were treated with 0.1% DMSO or Astaxanthin (30 μM) and then stimulated with RANKL (10 ng/mL) and M-CSF (30 ng/ml) for the indicated number of days. The expressed mRNA levels of (A) NFATc1, (B) TRAP, (C) DC-STAMP, and (D) cathepsin K were analyzed by real-time PCR compared with the DMSO control. * p <0.05, ** p <0.01, *** p <0.001 (n = 3).
Figure 2 Astaxanthin inhibits the expression of the genes involved in osteoclastogenesis. BMMs were treated with 0.1% DMSO or Astaxanthin (30 μM) and then stimulated with RANKL (10 ng/mL) and M-CSF (30 ng/ml) for the indicated number of days. The expressed mRNA levels of (A) NFATc1, (B) TRAP, (C) DC-STAMP, and (D) cathepsin K were analyzed by real-time PCR compared with the DMSO control. * p <0.05, ** p <0.01, *** p <0.001 (n = 3).CC BY · PubMed Central
Figure 3 BMMs were pretreated with 0.1%DMSO or Astaxanthin (30 μM) for 1 h and then stimulated with RANKL (10 ng/mL) and M-CSF (30 ng/mL) for the indicated time. Cell lysates were resolved by SDS-PAGE, and western blotting was performed with anti-NFATc1 and actin antibodies as indicated.
Figure 3 BMMs were pretreated with 0.1%DMSO or Astaxanthin (30 μM) for 1 h and then stimulated with RANKL (10 ng/mL) and M-CSF (30 ng/mL) for the indicated time. Cell lysates were resolved by SDS-PAGE, and western blotting was performed with anti-NFATc1 and actin antibodies as indicated.CC BY · PubMed Central
Figure 4 Experimental protocol for the induction and therapy of osteoporosis along with the treatment scheme.
Figure 4 Experimental protocol for the induction and therapy of osteoporosis along with the treatment scheme.CC BY · PubMed Central
Figure 5 Effect of AST on body weight and uterus weight. The (A) body weight and (B) uterus weight measured at 24 h after the last treatment. Each value represents the mean ± SD for n = 5. # p < 0.05, ## p < 0.01, and ### p < 0.001 SHAM group vs. OVX group. * p < 0.05, ** p < 0.01, and *** p < 0.001 OVX group vs. E2, AST 5, and AST 10 group.
Figure 5 Effect of AST on body weight and uterus weight. The (A) body weight and (B) uterus weight measured at 24 h after the last treatment. Each value represents the mean ± SD for n = 5. # p < 0.05, ## p < 0.01, and ### p < 0.001 SHAM group vs. OVX group. * p < 0.05, ** p < 0.01, and *** p < 0.001 OVX group vs. E2, AST 5, and AST 10 group.CC BY · PubMed Central
Figure 6 Effect of AST on serum biochemical markers. In the control, SHAM-operated mice and OVX mice with or without the administration of AST (5 and 10 mg/kg/day, p.o.) for 6 weeks, the serum (A) calcium, (B) phosphorus, (C) alkaline phosphatase, and (D) total cholesterol were determined by using a diagnostic slide. Each value represents the mean ± SD for n = 5. ## p < 0.01 and ### p < 0.001 SHAM group vs. OVX group. * p < 0.05 and *** p < 0.001 OVX group vs. E2, AST 5, and AST 10 group.
Figure 6 Effect of AST on serum biochemical markers. In the control, SHAM-operated mice and OVX mice with or without the administration of AST (5 and 10 mg/kg/day, p.o.) for 6 weeks, the serum (A) calcium, (B) phosphorus, (C) alkaline phosphatase, and (D) total cholesterol were determined by using a diagnostic slide. Each value represents the mean ± SD for n = 5. ## p < 0.01 and ### p < 0.001 SHAM group vs. OVX group. * p < 0.05 and *** p < 0.001 OVX group vs. E2, AST 5, and AST 10 group.CC BY · PubMed Central
Figure 7 Effect of AST on serum tartrate-resistant acid phosphatase (TRAP) in the control, SHAM-operated mice and OVX mice with or without the administration of AST (5 and 10 mg/kg/day, p.o.) for 6 weeks. Serum TRAP was measured by ELISA kit. Each value represents the mean ± SD for n = 5. Group numbers (1 = SHAM, 2 = OVX, 3 = AST 5 mg/kg, 4 = 10 mg/kg).
Figure 7 Effect of AST on serum tartrate-resistant acid phosphatase (TRAP) in the control, SHAM-operated mice and OVX mice with or without the administration of AST (5 and 10 mg/kg/day, p.o.) for 6 weeks. Serum TRAP was measured by ELISA kit. Each value represents the mean ± SD for n = 5. Group numbers (1 = SHAM, 2 = OVX, 3 = AST 5 mg/kg, 4 = 10 mg/kg).CC BY · PubMed Central
Figure 8 Effect of AST on trabecular morphometric parameters in proximal tibia of C3H/HeN mice. The mice were treated with the vehicle, AST (5 and 10 mg/kg/day, p.o.) for 6 weeks. (A) The three-dimensional micro-computed tomography images were analyzed by CTvol. (B) Tissue volume (TV), (C) bone volume (BV), (D) bone volume/tissue volume, (E) bone surface, (F) bone surface/tissue volume, (G) trabecular pattern factor, (H) structure model index, (I) trabecular thickness, (J) trabecular number, and (K) trabecular separation as analyzed with micro-CT Skyscan CTAn software. Each value represents the mean ± SD for n = 5. ## p < 0.01 and ### p < 0.001 SHAM group vs. OVX group. * p < 0.05 and *** p < 0.001 OVX group vs. E2, AST 5, and AST 10 group.
Figure 8 Effect of AST on trabecular morphometric parameters in proximal tibia of C3H/HeN mice. The mice were treated with the vehicle, AST (5 and 10 mg/kg/day, p.o.) for 6 weeks. (A) The three-dimensional micro-computed tomography images were analyzed by CTvol. (B) Tissue volume (TV), (C) bone volume (BV), (D) bone volume/tissue volume, (E) bone surface, (F) bone surface/tissue volume, (G) trabecular pattern factor, (H) structure model index, (I) trabecular thickness, (J) trabecular number, and (K) trabecular separation as analyzed with micro-CT Skyscan CTAn software. Each value represents the mean ± SD for n = 5. ## p < 0.01 and ### p < 0.001 SHAM group vs. OVX group. * p < 0.05 and *** p < 0.001 OVX group vs. E2, AST 5, and AST 10 group.CC BY · PubMed Central
Figure 9 Effect of AST on trabecular morphometric parameters in distal femur of C3H/HeN mice. The mice were treated with the vehicle, AST (5 and 10 mg/kg/day, p.o.) for 6 weeks. (A) The three-dimensional micro-computed tomography images were analyzed by CTvol. (B) Tissue volume (TV), (C) bone volume (BV), (D) bone volume/tissue volume, (E) bone surface, (F) bone surface/tissue volume, (G) trabecular pattern factor, (H) structure model index, (I) trabecular thickness, (J) trabecular number, and (K) trabecular separation as analyzed with micro-CT Skyscan CTAn software. Each value represents the mean ± SD for n = 5. ## p < 0.01 and ### p < 0.001 SHAM group vs. OVX group. * p < 0.05, ** p < 0.01, and *** p < 0.001 OVX group vs. E2, AST 5, and AST 10 group.
Figure 9 Effect of AST on trabecular morphometric parameters in distal femur of C3H/HeN mice. The mice were treated with the vehicle, AST (5 and 10 mg/kg/day, p.o.) for 6 weeks. (A) The three-dimensional micro-computed tomography images were analyzed by CTvol. (B) Tissue volume (TV), (C) bone volume (BV), (D) bone volume/tissue volume, (E) bone surface, (F) bone surface/tissue volume, (G) trabecular pattern factor, (H) structure model index, (I) trabecular thickness, (J) trabecular number, and (K) trabecular separation as analyzed with micro-CT Skyscan CTAn software. Each value represents the mean ± SD for n = 5. ## p < 0.01 and ### p < 0.001 SHAM group vs. OVX group. * p < 0.05, ** p < 0.01, and *** p < 0.001 OVX group vs. E2, AST 5, and AST 10 group.CC BY · PubMed Central
Figure 10 Effect of AST on bone mineral density (BMD) of trabecular in distal femur and proximal tibia of C3H/HeN mice in the control, SHAM-operated mice and OVX mice with or without the administration of AST (5 and 10 mg/kg/day, p.o.) for 6 weeks. (A) The femur BMD and (B) tibia BMD were analyzed by CTAn software. ### p < 0.001 SHAM group vs. OVX group. * p < 0.05, ** p < 0.01, and *** p < 0.001 OVX group vs. E2, AST 5, and AST 10 group.
Figure 10 Effect of AST on bone mineral density (BMD) of trabecular in distal femur and proximal tibia of C3H/HeN mice in the control, SHAM-operated mice and OVX mice with or without the administration of AST (5 and 10 mg/kg/day, p.o.) for 6 weeks. (A) The femur BMD and (B) tibia BMD were analyzed by CTAn software. ### p < 0.001 SHAM group vs. OVX group. * p < 0.05, ** p < 0.01, and *** p < 0.001 OVX group vs. E2, AST 5, and AST 10 group.CC BY · PubMed Central
Figure 11 Effect of AST on bone tissue of trabecular in distal femur of C3H/HeN mice. The mice were treated with the vehicle, AST (5 and 10 mg/kg/day, p.o.), for 6 weeks. (A) Histological analysis of distal femur with hematoxylin and eosin (H&E) and tartrate-resistant acid phosphatase (TRAP) staining; (B) Trabecular and (C) TRAP positive cells in femur were analyzed by Image J program. Each value represents the mean ± SD for n = 3. ### p < 0.001 SHAM group vs. OVX group. ** p < 0.01 and *** p < 0.001 OVX group vs. E2, AST 5, and AST 10 group.
Figure 11 Effect of AST on bone tissue of trabecular in distal femur of C3H/HeN mice. The mice were treated with the vehicle, AST (5 and 10 mg/kg/day, p.o.), for 6 weeks. (A) Histological analysis of distal femur with hematoxylin and eosin (H&E) and tartrate-resistant acid phosphatase (TRAP) staining; (B) Trabecular and (C) TRAP positive cells in femur were analyzed by Image J program. Each value represents the mean ± SD for n = 3. ### p < 0.001 SHAM group vs. OVX group. ** p < 0.01 and *** p < 0.001 OVX group vs. E2, AST 5, and AST 10 group.CC BY · PubMed Central

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Metadata

Authors
Hwang, Y.-H., Kim, K.-J., Kim, S.-J., Mun, S.-K., Hong, S.-G., Son, Y.-J., & Yee, S.-T.
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2018-03-19
Volume
19
Issue
3
Pages
912
ISSN
1422-0067
DOI
10.3390/ijms19030912
PMC
PMC5877773
Cited by
48
References
4
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)

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Hwang, Y.-H., Kim, K.-J., Kim, S.-J., Mun, S.-K., Hong, S.-G., Son, Y.-J., & Yee, S.-T. (2018). Suppression Effect of Astaxanthin on Osteoclast Formation In Vitro and Bone Loss In Vivo. International Journal of Molecular Sciences. https://doi.org/10.3390/ijms19030912

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