| Objective To explore the curative effect and mechanism of the strong-bone and analgesic prescription on interfering with osteoporosis in castrated rats by regulating bone resorption and osteoclastic activity, and to provide a feasible strategy for the clinical treatment of postmenopausal osteoporosis. Methods Forty SD rats were randomly divided into the following groups: the strong-bone and analgesic prescription group, estradiol group, model group, and sham surgery group. All groups, except for the sham surgery group, were constructed according to the internationally recognized postmenopausal osteoporosis (PMOP) model. Seventh day after modeling, the rats were respectively given Chinese medicine liquid, estradiol, and distilled water by gavage. After the final collection, bone mineral density of the right femur of the rats was measured. The pathological morphology of the tibial bone tissue of each group was observed using HE staining. The serum levels of E2 and RANKL were detected with ELISA. The protein expressions of RANK, TRAP, and CTSK were analyzed using immunohistochemistry. Results Compared with the castrated rat model group, the group treated with the strong-bone and analgesic prescription showed an increase in bone mineral density, improvement in the microstructure of the tibial and femoral bone tissue, slight restoration of trabecular bone continuity, reduction in the size of the bone marrow cavity, and decrease in the number of adipose vacuoles. The expression of E2 in serum was up-regulated. The level of RANKL was down-regulated. The protein expressions of RANK, TRAP, and CTSK in the bone tissue were also down-regulated (P<0.05). Conclusion The strong-bone and analgesic prescription reduces the expressions of relevant osteoclast factors in castrated rat. It inhibits over-differentiation and excessive bone absorption activity of osteoclasts, restores bone-coupling imbalance, thereby exerting therapeutic effect on postmenopausal osteoporosis. |