RESUMO
Objective To investigate the change of levels of related cytokines,including transforming growth factor-β2 (TGF-β2),basic fibroblast growth factor (bFGF),platelet-derived growth factor (PDGF),interleukin-6 (IL-6),interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α) and behavior in streptozotocin-induced diabetic rats between the before and after fracture,at the same time,to analyse the relativity of them.Methods The rat models of diabetic were induced by intraperitoneal injection of streptozotocin,which were divided into different diabetes mellitus group (DM group) randomly.The right tibiofibula of all the rats of diabetes mellitus group and normal control group(NC group) were broken,and then treated with external fixation.The bone callus formation was evaluated by X-ray.When all the operation above was completed,the rats were domesticated in different cages.The concentration of related cytokines of the DM groups and NC group was detected at different time.Results The behavior changes of diabetes fracture rats were distinct and appeared a series symptoms such as bradykinesia,dull,polydipsia,polyphage,polyuria,emaciated obviously.The concentration of related cytokines (TGFβ2,BFGF,PDGF,IL-6,IL-8 and TNF-α) of the two groups was detected at 1,2 and 4 weeks.The difference between them was significantly(TNF-α:the concentration of NC group were (9.87 ± 1.06) ng/ml,(14.07 ± 1.43)ng/ml and(12.02 ± 1.02) ng/ml; the concentration of DM group were (11.65 ± 1.18) ng/ml,(16.29 ± 1.24)ng/ml and(13.87 ± 1.25)ng/ml ; P ＜ 0.05).X-ray films showed that the fracture healing of NC group was more superior than that of DM group.Conclusion The reduction of TGF-β2,BFGF,PDGF and the increase of IL-6,IL-8,TNF-α in early fracture are one of important reasons for delayed union and nonunion in diabetic rats.At the same time,there is a cooperative action between them.Dynamic observation of the concentration of related cytokines will provide eliable experimental data to estimate fracture healing,delayed union and nonunion.It is favourable to acquaint the regulatory mechanism of fracture healing at molecular level.