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目的探讨创伤性脑损伤影响骨折愈合速度的可能机制。方法采用创伤性脑损伤合并一侧胫骨骨折(A组)制作多发伤模型,不同时点观察FOS、JUN、bFGF、VEGF表达并与B组(单纯一侧胫骨骨折)比较,X线观察骨折愈合情况。结果正常小鼠脑组织FOS、JUN、bFGF、VEGF低水平表达,B组略强。A组脑组织FOS和JUN的表达具有时程的一致性,创伤性脑损伤(TBI)后3 h达到高峰,12 h以后降至对照水平;bFGF与VEGF分别于创伤性脑损伤后12 h、24 h达到高峰,72 h降至对照水平。两组骨折位点FOS、JUN表达均于6 h达峰值,24 h后降至对照水平。3 h、6 h、12 h组间比较差异有显著性。A组骨折位点bFGF、VEGF表达分别于12 h、24 h达峰值,B组于2,4 h、48 h达峰值,均持续表达96 h以上。Spearman等级相关分析发现,A组脑挫伤灶周围脑组织FOS蛋白与bFGF表达、bFGF与VEGF蛋白表达呈正相关,相关系数分别是0.896、0.832(P<0.05);A组骨折位点FOS蛋白与bFGF表达、bFGF与VEGF蛋白表达呈正相关,相关系数分别是0.938、0.945(P<0.05);B组骨折位点FOS蛋白与bFGF表达、bFGF与VEGF蛋白表达也呈正相关,相关系数分别是0.833、0.914(P<0.05);两组脑组织FOS、JUN蛋白与骨折位点FOS、JUN表达的关系无统计学意义。影像学上A组在术后第三周时已接近全部愈合,B组到第4周时才全部愈合。结论创伤性脑损伤合并长骨骨折足比较理想的多发伤实验动物模型;创伤性脑损伤后骨折位点bFGF、VEGF表达更早更强,促进成骨。
Objective To investigate the possible mechanism of traumatic brain injury affecting fracture healing. Methods The traumatic brain injury combined with tibial fracture on one side (group A) was used to make multiple trauma models. The expression of FOS, JUN, bFGF and VEGF were observed at different time points. Compared with group B (only one tibial fracture), fracture healing Happening. Results In normal mice, the expression of FOS, JUN, bFGF and VEGF were low in the brain tissue, but slightly in the B group. The expression of FOS and JUN in group A was consistent with the time course. The peak at 3 h after traumatic brain injury (TBI) peaked at 12 h and then decreased to the control level. The expression of bFGF and VEGF was increased at 12 h after traumatic brain injury, Reached the peak at 24 h and dropped to the control level at 72 h. The expression of FOS and JUN at the fracture sites in both groups peaked at 6 h and dropped to the control level after 24 h. 3 h, 6 h, 12 h groups were significantly different. The expression of bFGF and VEGF in group A were peaked at 12 h and 24 h, respectively, and peaked at 2, 4 and 48 h in group B, all of which persisted for more than 96 h. Spearman rank correlation analysis showed that there was a positive correlation between the expression of FOS protein and bFGF and the expression of bFGF and VEGF in brain tissue of group A, the correlation coefficients were 0.896,0.832 (P <0.05) respectively. In group A, the expression of FOS protein and bFGF The expression of bFGF and VEGF protein was positively correlated with the correlation coefficient of 0.938 and 0.945 respectively (P <0.05). The expression of FOS protein and bFGF in the fracture site of group B was also positively correlated with the expression of bFGF and VEGF protein, the correlation coefficient was 0.833,0.914 (P <0.05). There was no significant correlation between the expression of FOS and JUN in the two groups of brain tissues and the expression of FOS and JUN in the fracture sites. A group of patients in the third week after surgery almost all healed, B group until the 4th week when all healed. Conclusion Traumatic brain injury combined with long bone fracture is an ideal animal model of multiple traumatic injury. The expression of bFGF and VEGF in traumatic brain injury is earlier and stronger than that in long bone fracture.