Objective To investigate the effect of salidroside on postmenopausal osteoporosis by activating PI3K/Akt pathway. Methods The rat model of postmenopausal osteoporosis was established and randomly divided into model group, LY294002 (PI3K/Akt pathway inhibitor) group, salidroside group and salidroside + LY294002 group, with 12 in each group, another 12 were set as sham operation group. After treatment, the elastic modulus, the maximum load and the yield load of the biomechanical index of the femur of the rats were measured with the orthopedic biomechanical tester; the mineral salt content of femur was measured; hematoxylin eosin (HE) staining was used to detect the pathological changes of bone tissue; the levels of serum IL-6 and TNF-α were detected by enzyme-linked immunosorbent assay (ELISA); and the expression of PI3K/Akt pathway related proteins was detected by Western blot. Results Compared with the sham operation group, the bone tissue of the model group showed sparsely broken trabeculae, the number of trabeculae was significantly reduced, and there were many spaces, unable to connect into nets and other pathological damages, the levels of serum IL-6 and TNF-α increased significantly (P<0.05), while the elastic modulus, maximum load, yield load of femur, mineral salt content of bone, and levels of p-PI3K/PI3K and p-Akt/Akt in bone tissue decreased significantly (P<0.05); compared with the model group, the pathological injury of bone tissue in salidroside group was reduced, the levels of serum IL-6 and TNF-α decreased (P<0.05), while the elastic modulus, maximum load, yield load of femur, mineral salt content of bone, and levels of p-PI3K/PI3K and p-Akt/Akt in bone tissue increased significantly (P< 0.05); in LY294002 group, the pathological injury of bone tissue was aggravated, the levels of serum IL-6 and TNF-α were significantly increased (P<0.05), while the elastic modulus, maximum load, yield load of femur, mineral salt content of bone, and levels of p-PI3K/PI3K and p-Akt/Akt in bone tissue decreased significantly (P< 0.05). Compared with LY294002 group, the pathological injury of bone tissue in salidroside + LY294002 group was reduced, the levels of serum IL-6 and TNF-α were significantly decreased (P<0.05), while the elastic modulus, maximum load, yield load of femur, mineral salt content of bone, and levels of p-PI3K/PI3K and p-Akt/Akt in bone tissue increased significantly (P<0.05). Compared with salidroside group, the pathological injury of bone tissue in salidroside + LY294002 group was aggravated, the levels of serum IL-6 and TNF-α were significantly increased (P <0.05), while the elastic modulus, maximum load, yield load of femur, mineral salt content of bone, and levels of p-PI3K/PI3K and p-Akt/Akt in bone tissue decreased significantly (P<0.05). Conclusion Salidroside may improve postmenopausal osteoporosis by activating PI3K/Akt pathway. |