| Objective To observing the inhibitory effect of sodium alendronate on bone loss in ovariectomized rats and to explore the mechanism of its inhibitory effect on bone loss. Methods Forty female Wistar rats were randomly divided into sham surgery group (n=10) and modeling group (n=30). Rats in the modeling group underwent minimally invasive abdominal resection of bilateral ovaries. Rats in the sham surgery group underwent excision of equal volume of adipose tissue. Three days later, rats in the modeling group of were randomly divided into three groups: the model group (OVX), the positive drug ethinylestradiol group (EE), and the alendronate sodium group. Rats of each group received medication or distilled water by gavage with the prescribed dosage. After significant differences in overall bone mineral density among the groups of rats were observed, all rats were euthanized. After dissection, each organ of the rats was weighed and the organ coefficients were calculated. Dual energy X-ray absorptiometry was used to detect the bone mineral density of the rat femur and the vertebral bone. AG-IS universal testing machine was used to detect the biomechanics of the rat femur. VG staining method was used for bone morphometric analysis. Blood was collected from the abdominal aorta of rats and serum was separated. ELISA kit was used to analyze osteocalcin (OC) and tartaric acid phosphatase (TRACP 5b) levels in rat serum. Results Compared with the sham group, there was no significant change in the body weight of the other groups of rats. The organ index results showed that compared with the sham group, there were no significant changes in the liver, lung, spleen, and kidney indices of each group of rats, while the uterine index of the model group rats reduced significantly compared to the control group. After intervention with ethinylestradiol or alendronate sodium, the uterine index of the model group rats increased significantly. The bone mineral density results showed that after modeling, the bone mineral density of the whole body, femur, and vertebrae in rats significantly decreased. However, after intervention with alendronate sodium, bone mineral density significantly increased, but it could not return to normal state. In biomechanical experiments, the maximum load on the femur and vertebrae showed a trend similar to bone mineral density. There was no significant change in the elastic modulus values among the groups before and after administration. The results of bone morphometry showed a significant increase in the number and density of bone trabeculae in the EE group and the alendronate sodium group. In ovariectomized rats, serum levels of osteocalcin (OC) reduced significantly and levels of TRACP 5b increased significantly. However, after administration of ethinylestradiol or alendronate sodium, the OC level in the EE group increased and the TRACP 5b content significantly decreased. The OC level in the alendronate sodium group continued to decrease and TRACP 5b content also significantly decreased. The difference was statistically significant. Conclusion Alendronate sodium increases bone mineral density and bone mass after castration and inhibits bone loss in ovariectomized rats. Its main mechanism of action may be achieved by inhibiting bone resorption by osteoclasts, with a weak effect on bone formation. |