Abstract

To explore beta-sitosterol involved in regulating the mechanism of postmenopausal osteoporosis in the elderly through the phosphoinositide-3-kinase–protein kinase B. 90 Sprague Dawley grade female rats were selected as the research subjects and randomly divided into a control, beta-sitosterol treatment, and the model group. Establishing an elderly postmenopausal osteoporosis model using oophorectomy, beta-sitosterol treatment group was given 20 μmol/l, the model group and control group were given equal volume of 0.9 % physiological saline by gavage of sitosterol drugs. In terms of bone mineral density, the bone mineral density in the beta-sitosterol group was raised than that in the model group. The results of hematoxylin and eosin staining showed that the degree of osteoporosis in the beta-sitosterol group was less than that in the model group. Enzyme-linked immunosorbent assay results showed that the concentrations of serum estradiol, bone alkaline phosphatase, osteocalcin and procollagen N-terminal propeptide in the beta-sitosterol group were raised than those in the model group. Quantitative polymerase chain reaction results showed that the expression of phosphoinositide- 3-kinase–protein kinase B messenger ribonucleic acid in bone tissue of beta-sitosterol treated group was raised than that of model group. Western blot analysis showed that the expression of phosphoinositide-3- kinase–protein kinase B was increased in beta-sitosterol treated group. Further experiments confirmed that the protective effect of beta-sitosterol on senile postmenopausal osteoporosis could be reversed by inhibiting phosphoinositide-3-kinase–protein kinase B. Beta-sitosterol can regulate senile postmenopausal osteoporosis and regulate the expression of bone mineral density and osteogenesis-related factors through phosphoinositide- 3-kinase–protein kinase B signal pathway.