Effect of Erzhi Wan on Bone Metabolism in Rats with Ovariectomized Osteoporosis

OBJECTIVE To clarify the regulating effect of Erzhi Wan (EZW) on bony reconstitution in ovariectomized osteoporosis rats and explore its mechanism. METHODS The animal model of postmenopausal osteoporosis (PMOP) was made by ovariectomy. After confirming the success of the model， 60 model rats were randomly divided into 6 groups， including model group， alendronate sodium group， sodium fluoride group， EZW group， Ligustrum lucidum group and Eclipta group， 10 rats were set up in the sham operation group. Each group was given， physiological saline (5 mL/kg)， alendronate sodium (1 mg/kg)， sodium fluoride (5 mg/kg)， EZW (2 g/kg)， Ligustrum lucidum (1 g/kg) and Eclipta (1 g/kg) intragastric administrated once a day for 8 weeks， the intragastric administrated of the sham operation group was the same as that of the model group. Scanning rat femur with Micro-CT; Bone mineral density (BMD) of femoral neck was measured by dual energy X-ray absorptiometry; the maximum load of bone was measured by vertebral compression; Serum bone alkaline phosphatase (BALP)， tartrate-resistant acid phosphatase-5b (TRACP-5b)， nuclear factor κB receptor activating factor ligand (RANKL)， osteoprotectin (OPG)， β-catenin and chemerin were detected by ELISA method; qPCR was used to detect bone tissue RANKL， OPG， β-catenin and chemerin gene expression. RESULTS EZW， Ligustrum lucidum and Eclipta significantly increased bone mass， bone maximum load， and repaired bone microstructure.In the serum， EZW， Ligustrum lucidum and Eclipta significantly reduced the expression levels of TRACP-5b， RANKL and chemerin， and increased the expression levels of BALP， OPG， β-catenin. In the bone tissue， EZW， Ligustrum lucidum and Eclipta group significantly inhibited the expression of RANKL and chemerin mRNA and promoted the increase of OPG and β-catenin mRNA expression. CONCLUSION EZW can effectively intervene the abnormal bone metabolism in ovariectomized osteoporosis rats， and its mechanism is closely related to the regulation of chemerin.