Salidroside Alleviates Diabetic Osteoporsis Through AKT/GSK3β Pathway

ObjectiveSalidroside can significantly improve osteoporosis caused by various causes,but its protective effect on diabetic osteoporosis(DOP)is rarely reported.The purpose of this study was to explore the preventive and therapeutic effects and potential mechanisms of salidroside on DOP.MethodsSprague Dawley(SD)rats were intraperitoneally injected with streptozotocin(STZ)to establish type I diabetic models.Rats were randomly divided into three groups: CON group(control group);DM group(diabetes rats);DM-SAL group(diabetic rats with salidroside treatment).Von Kossa staining was used to observe the micromorphology of the femoral trabecula,dual-energy X-ray absorptiometry was used to measure the density of the femur,the serum alkaline phosphatase(ALP)and calcium and phosphorus content were detected by the kit,and the expressions of AKT,p-AKT,GSK3,p-GSK3β and BMP-2 in bone tissue were detected by Western blot.Molecular docking between salidroside and BMP-2 was also explored.ResultsCompared with CON group,DM group showed decreased trabecular area,thickness,number,and bone density,together with decreased ratio of bone ash weight to wet weigh,serum ALP,and p-AKT/AKT,p-GSK3β/GSK3β and BMP-2expression,while,increased calcium and phosphorus(P<0.05).Salidroside treatment could significantly reverse the changes of these parameters induced by diabetes.The difference between DM-SAL group and DM group was statistically significant(P<0.05).The binding energy of salidroside and BMP-2 is-0.35,indicating closely combination.ConclusionsSalidroside may activate AKT/GSK3β pathway by up-regulating the expression of BMP-2 to alleviate DOP.