| Objective To explore the effect of panax notoginseng saponins (PNS) regulating receptor for advanced glycation end products (RAGE)/mitogen activated protein kinase (MAPK) signaling pathway on inflammatory damage in rats with diabetic osteoporosis (DOP). Methods SD rats were divided into control group, model group, metformin (MET) group (100 mg/kg), PNS low dose group (PNS-L group, 10 mg/kg PNS), PNS high dose group (PNS-H group, 20 mg/kg PNS), PNS-H+empty vector plasmid group (20 mg/kg PNS+15 μL empty vector plasmid), and PNS-H+RAGE overexpression group (20 mg/kg PNS+15 μL RAGE overexpression plasmid). Except for rats in the control group, the rats in other groups were fed with high sugar and high fat diet and intraperitoneal injection of streptozotocin to construct the DOP model. After successful modeling, rats in each group was treated with corresponding drug administration. Bone mineral density (BMD) of the rat femur was measured with dual energy X-ray absorptiometry. Fasting blood glucose (FBG), serum fasting insulin (FINS), tartrate resistant acid phosphatase (TRACP), alkaline phosphatase (ALP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) were measured with blood glucose tester and enzyme-linked immunosorbent assay. Three-point bending test and hematoxylin eosin staining were used to detect the changes of femur biomechanics and pathological morphology. Western blotting was used to detect the expression of RAGE/MAPK pathway proteins. Results Compared with those in the model group, the femoral trabeculae in MET group, PNS-L group, and PNS-H group increased and the spacing decreased, and the fracture was alleviated, the femur BMD, FINS, ALP, maximum load and stiffness of femur significantly increased, and the expression levels of FBG, TRACP, IL-6, TNF-α, femoral tissue RAGE, and p-p38 MAPK/p38 MAPK protein significantly decreased (P<0.05). RAGE overexpression could reverse the improvement effect of PNS-H on DOP rats (P<0.05). Conclusion PNS alleviates the inflammatory damage in DOP rats by inhibiting the RAGE/MAPK signaling pathway. |