Objective To analyze the regulatory mechanism of semaglutide on bone metabolism and inflammatory factors in diabetic osteoporosis (DOP) rats. Methods Forty-five SD rats were randomly divided into 3 groups, blank group, model group and semaglutide group, with 15 rats in each group. The serum FBG, FINS, inflammatory factors, bone mineral density, bone metabolism indexes, p-PI3 K, PI3 K, pAkt, Akt protein levels, biomechanical related parameters, HE staining of femoral tissue, TRAP staining of femoral tissue, and HE staining of adipose tissue were compared among the three groups. Results The size of adipocytes in the blank group was uniform, the structure was clear, and the structure was relatively complete, but the infiltration of inflammatory cells was significantly reduced. Compared to those in the blank group, the average number of osteoclasts / bone surface, TRAP, OC, Ca, ALP, P, FBG, TNF-α, and IL-6 in the model group increased significantly (P<0.05). Compared to those in the model group, the average number of osteoclasts/bone surface, TRAP, OC, Ca, ALP, P, FBG, FINS, TNF-α, and IL-6 in the smeglutide group decreased significantly (P<0.05). Compared to those in the blank group, bone mineral density, FINS, p-PI3K/PI3K, p-Akt/Akt, femoral elastic modulus, maximum stress, maximum load, and elastic load of the model group reduced significantly (P<0.05). Compared to those in the model group, bone mineral density, FINS, p-PI3K/PI3K, p-Akt/Akt, femoral elastic modulus, maximum stress, maximum load, and elastic load of the semaglutide group increased significantly (P<0.05). Conclusion Semaglutide effectively improves bone metabolism and inflammatory response in DOP rats. Its mechanism may be related to the activation of PI3K/Akt pathway. |