Xu M T, Sun S, Zhang L, Xu F, Du S L, Zhang X D, Wang D W
Department of Joint Surgery, Shandong Provincial Hospital, Shandong University, Jinan, Shandong Province, China.
Department of Orthopaedics, Liaocheng People's Hospital, Liaocheng Clinical School, Taishan Medical University, Liaocheng, Shandong Province, China.
Braz J Med Biol Res. 2016 Jan;49(1):e4736. doi: 10.1590/1414-431X20154736. Epub 2015 Nov 27.
Transforming growth factor beta 1 (TGF-β1) and bone morphogenetic protein-2 (BMP-2) are important regulators of bone repair and regeneration. In this study, we examined whether TGF-β1 and BMP-2 expressions were delayed during bone healing in type 1 diabetes mellitus. Tibial fractures were created in 95 diabetic and 95 control adult male Wistar rats of 10 weeks of age. At 1, 2, 3, 4, and 5 weeks after fracture induction, five rats were sacrificed from each group. The expressions of TGF-β1 and BMP2 in the fractured tibias were measured by immunohistochemistry and quantitative reverse-transcription polymerase chain reaction, weekly for the first 5 weeks post-fracture. Mechanical parameters (bending rigidity, torsional rigidity, destruction torque) of the healing bones were also assessed at 3, 4, and 5 weeks post-fracture, after the rats were sacrificed. The bending rigidity, torsional rigidity and destruction torque of the two groups increased continuously during the healing process. The diabetes group had lower mean values for bending rigidity, torsional rigidity and destruction torque compared with the control group (P<0.05). TGF-β1 and BMP-2 expression were significantly lower (P<0.05) in the control group than in the diabetes group at postoperative weeks 1, 2, and 3. Peak levels of TGF-β1 and BMP-2 expression were delayed by 1 week in the diabetes group compared with the control group. Our results demonstrate that there was a delayed recovery in the biomechanical function of the fractured bones in diabetic rats. This delay may be associated with a delayed expression of the growth factors TGF-β1 and BMP-2.
转化生长因子β1(TGF-β1)和骨形态发生蛋白-2(BMP-2)是骨修复和再生的重要调节因子。在本研究中,我们检测了1型糖尿病患者在骨愈合过程中TGF-β1和BMP-2的表达是否延迟。对95只10周龄的成年雄性糖尿病Wistar大鼠和95只对照成年雄性Wistar大鼠造成胫骨骨折。在骨折诱导后的第1、2、3、4和5周,每组处死5只大鼠。通过免疫组织化学和定量逆转录聚合酶链反应测量骨折后前5周每周骨折胫骨中TGF-β1和BMP2的表达。在处死大鼠后,还在骨折后第3、4和5周评估愈合骨的力学参数(弯曲刚度、扭转刚度、破坏扭矩)。两组的弯曲刚度、扭转刚度和破坏扭矩在愈合过程中持续增加。与对照组相比,糖尿病组的弯曲刚度、扭转刚度和破坏扭矩的平均值较低(P<0.05)。术后第1、2和3周,对照组中TGF-β1和BMP-2的表达明显低于糖尿病组(P<0.05)。与对照组相比,糖尿病组中TGF-β1和BMP-2表达的峰值水平延迟了一周。我们的结果表明,糖尿病大鼠骨折骨的生物力学功能恢复延迟。这种延迟可能与生长因子TGF-β1和BMP-2的表达延迟有关。