curcumin and Femoral-Fractures

BACKGROUND Bone fracture, a common injury to bones leads to various biophysiological changes and pathological responses in the body. The current study investigated curcumin for treatment of bone fracture in a rat model of bone trauma, and evaluated the related mechanism. MATERIAL AND METHODS The rats were separated randomly into 3 groups; sham, model, and curcumin treatment groups. The fracture rat model was established by transverse osteotomy in the right femur bone at the mid-shaft. The osteoblast count was determined using hematoxylin and eosin staining. Vascular endothelial growth factor (VEGF) and proliferating cell nuclear antigen (PCNA) expression were measured by western blotting. RESULTS The rpS6-phosphorylation was suppressed and light chain 3 (LC3II) expression elevated in the curcumin treated group of the fracture rat model. In the curcumin-treated group, mineralization of fracture calluses was markedly higher on day 14 of fracture. The formation of osteoblasts was observed at a greater rate in the curcumin treated group compared to the model rat group. Treatment of rats with curcumin significantly (P<0.05) promoted expression of PCNA and VEGF. The decrease in CD11b+/Gr-1+ cell expansion in rats with bone trauma was alleviated significantly by curcumin treatment. A marked increase in arginase-1 expression in rats with bone trauma was caused by curcumin treatment. CONCLUSIONS In summary, curcumin activates autophagy and inhibits mTOR activation in bone tissues of rats with trauma. The curcumin promoted myeloid-derived suppressor cell (MDSC) proliferation and increased expansion of MDSCs in a rat model of trauma. Therefore, curcumin may have beneficial effect in patients with bone trauma and should be evaluated further for development of treatment.

Topics: Animals; Arginase; Bone and Bones; Bony Callus; CD11b Antigen; Cell Proliferation; Curcumin; Disease Models, Animal; Femoral Fractures; Male; Microtubule-Associated Proteins; Myeloid-Derived Suppressor Cells; Osteoblasts; Phosphorylation; Proliferating Cell Nuclear Antigen; Protective Agents; Rats, Sprague-Dawley; Ribosomal Protein S6; Vascular Endothelial Growth Factor A; Wounds and Injuries

To determine the radiologic, histologic and biomechanical effects of curcumin on bone healing using a total rat femur fracture injury model.. Sixty four male Wistar-Albino rats weighing 170-210 g were used in this study. The animals were randomly divided into eight groups and 5 or 6 animals were placed in each cage. A transverse femur shaft fracture model used. The animals in study groups received oral curcumin at a dose of 200 mg/kg for 14 days or 28 days. Remaining animals received only saline solution by oral gavage for a period of 14 days and 28 days as control groups. After sacrification the left femurs used for radiological, histological and biomechanical evaluation.. The groups treated with curcumin showed no significant difference in terms of radiological, histological and biomechanical evaluations in 14 days groups. Also there was no significant difference between curcumin and control groups for 28 days according to radiological, histological and biomechanical tests.. According to our results, curcumin has no positive effect on fracture healing not only histologically but also radiologically and biomechanically. Curcumin's antioxidant effect may be more noticeable with long term follow up investigation as it may have a positive effect in remodelling phase. Long term follow up designed studies may be planned to investigate its effect on remodelling phase of fracture healing.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Biomechanical Phenomena; Curcumin; Disease Models, Animal; Femoral Fractures; Femur; Fracture Healing; Male; Radiography; Rats; Rats, Wistar

BACKGROUND The aim of this study was to use a rat model of femoral fracture healing to study the effects of curcumin on cell autophagy, compared with treatment with 3-methyladenine (3-MA), an inhibitor of autophagy. MATERIAL AND METHODS Thirty-six Sprague-Dawley rats with right mid-femoral fracture were divided into three groups: the curcumin-treated group (N=12) (gavage with curcumin 400 mg/kg/day); the curcumin + 3-MA-treated group (gavage with curcumin 400 mg/kg/day + 3-MA 30 mg/kg/day); and the control group (N=12) (gavage normal saline). Each group underwent femoral bone imaging using anteroposterior X-ray and micro-computed tomography (CT) at two weeks and six weeks following bone fracture. All rats were euthanized at the end of the study. Histology of the bone was performed to compare bone healing. Immunofluorescence and immunohistochemical tissue staining and Western blots were performed, to compare the expression of autophagy-related proteins, Beclin-1 and LC3-II. RESULTS Autophagy of rat femoral bone tissue was activated following fracture, increasing with time, reaching a peak at 24 hours. Imaging and histology showed that curcumin promoted the fracture healing in rats, which was reduced by treatment with 3-MA. Immunohistochemistry, immunofluorescence, and Western blot showed that curcumin treatment increased the expression of Beclin-1 and LC3-II, which were reduced by treatment with the autophagy inhibitor, 3-MA. CONCLUSIONS The findings of this study, in a rat model of femoral bone fracture healing, showed that curcumin promoted bone healing and autophagy, which were reduced by treatment with 3-MA, a known inhibitor of autophagy.

Topics: Adenine; Animals; Autophagy; Bone and Bones; Curcumin; Femoral Fractures; Femur; Fracture Healing; Male; Models, Animal; Rats; Rats, Sprague-Dawley; X-Ray Microtomography