Abstract
BackgroundJSOG-6 is used as a traditional medicine to relieve the symptoms associated with inflammation, rheumatism, and osteoporosis in Korea. In the present study, we investigated the effects of JSOG-6 on bone loss prevention both in in vitro and in vivo as well as its underlying mechanism of action.MethodsProtection against bone loss was assessed in an ovariectomized (OVX) mouse model. Bone microarchitecture was measured using a micro-computed tomography to detect the parameters of three-dimensional structure of a trabecular bone. Serum biomarkers were also evaluated in an OVX-induced model. Osteoclasts derived from mouse bone marrow cells (BMCs) and osteoblastic MC3T3-E1 cells were also employed to investigate the mechanism of action.ResultsOral administration of JSOG-6 significantly increased the bone mineral density (BMD) of the femur in OVX mice in vivo. Especially, the reduced Tb.No (trabecular bone number) in the OVX group was significantly recovered by JSOG-6 treatment. The serum levels of alkaline phosphatase (ALP), osteocalcin, C-terminal telopeptide, and tartrate-resistant acid phosphatase, biomarkers of bone resorption, were significantly elevated in OVX mice, but JSOG-6 effectively inhibited the increase in OVX mice. JSOG-6 was also found to enhance the osteoblastic differentiation and maturation with the increase of the density and ALP activity, a marker of osteoblastic differentiation, as well as calcium deposition, a marker of osteoblastic maturation in MC3T3-E1 cells. The effects of JSOG-6 on osteoblastic differentiation were also associated in part with the increase of ALP and OPN mRNA expressions and the decrease of RANKL mRNA expression in MC3T3-E1 cells.ConclusionsThe findings demonstrate that JSOG-6 induced protection against bone loss in OVX mice, and its anti-osteoporotic property might be, in part, a function of the stimulation of osteoblast differentiation and the inhibition of osteoclast formation. These findings suggest that JSOG-6 might be an applicable therapeutic traditional medicine for the regulation of the osteoporotic response.
Highlights
JSOG-6 is used as a traditional medicine to relieve the symptoms associated with inflammation, rheumatism, and osteoporosis in Korea
Mice given an oral administration of JSOG-6 for 12 weeks after OVX showed a relatively slow increase in body weight compared to the OVX group
The bone mineral density (BMD) of the trabecular bone of the femur in mice treated with JSOG-6 (50 mg/kg) was shown to be 83.0% higher than that in the OVX group and was not significantly different from that in the Sham control group (P < 0.01)
Summary
JSOG-6 is used as a traditional medicine to relieve the symptoms associated with inflammation, rheumatism, and osteoporosis in Korea. Osteoporosis is an age-dependent metabolic bone disease characterized by the decrease in bone mass, the deterioration of bone tissue, and an increased risk of fractures [1,2]. Osteoclasts are derived from hematopoietic cells within the monocyte/macrophage lineage [7] and regulated by the combined action of the receptor activator of the NF-κB ligand (RANKL) [8]. Osteoblasts induce the increase in bone mass by inhibiting the ability of osteoclasts. Osteoblasts express RANKL and osteoprotegerin (OPG), a decoy receptor of RANKL, which are essential factors regulating the formation and activation of osteoclasts (osteoclastogenesis) [9,10]. Excessive osteoclastogenesis and defects in osteoblastogenesis are associated with bone diseases such as osteoporosis and rheumatoid arthritis [12]
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