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Compared with Sham rats, OVX significantly lowered bone volume fraction, by 87%, trabecular thickness by 14%, trabecular amount by 85% and connectivity density by 91%, and increased trabecular separation by 320%.



As shown in Figure 5A, serum BALP as a bone formation marker was significantly increased in OVX rats, while drug treatment Hedgehog inhibitor did not affect the increase. TRAP 5b in serum is proposed to be a marker for osteoclasts. As shown in Figure 5B, serum TRAP 5b was significantly increased in OVX rats compared with Sham group but was significantly attenuated in 30SM group, consistent with exchange in osteoclast number measured by histological assessment and indicating increased bone resorption. In order to understand the mechanism of SM on bone resportion parameter, malondialdehyde and nitric oxide were measured. OVX significantly increased serum MDA levels, meaning the induction of lipid peroxydation in OVX rats.

OVX significantly increased serum osteocalcin and ALP activity Hedgehog inhibitor and SM treatment did not affect the increase. OVX induced significant trabecular bone loss due to estrogen deficiency and subsequent increased bone turnover. SM at 30 mg/kg body weight/day dosage significantly attenuated trabecular bone loss and BMD decrease induced by OVX. SM can contribute to bone balance probably through preventing an increase in osteoclast number by decreasing osteoclast maturation. SM is a potential anti osteoporotic natural product. For several decades, SM has been widely used for the treatment of various microcirculatory disturbancerelated diseases, such as cardiovascular disease, cerebrovascular disease, liver dysfunction, renal deficiency and diabetic vascular complications.

Previous studies have showed that OVX condition induces liver inflammation. The estrogen induced prevention effect against bone loss may involve suppression of inflammatory cytokines such as IL 1, IL 6 or TNF a, which in turn activate inducible nitric oxide synthase.