人工硬脑膜对颅骨缺损修复的影响

Effect of artificial dura mater on cranial defect repair

摘要:

目的 通过分析大鼠颅盖骨缺损修复过程中体重的变化，以及骨形态发生蛋白2（BMP2）信号通路的表达变化规律，探索幼龄动物颅骨缺损修复机制。方法 采用10 d幼龄SD大鼠，以大鼠矢状缝为界，在右侧顶骨中心，直径约2 mm做一骨窗，去除骨瓣；空白组不进行任何处理；人工膜组将5 mm正方形人工硬脑膜置于缺损下。分别在第2、4及6周末处死动物并取材。每组6只。测量三组的生理学指标及检测骨缺损处BMP2、白细胞抑制因子1（Smad1）和矮小相关转录因子2（Runx2）的表达情况。结果 两组颅骨缺损面积均发生缩小，空白组在4周时骨缺损修复了造模面积的70%，在6周时修复了造模面积的86%；人工膜组在4周时骨缺损修复了造模面积的20%，在6周时修复了造模面积的36%。第2、4及6周末3个时间周期内（除4周人工膜组BMP2蛋白与空白组无统计学差异外），人工膜组BMP2、Smad1、Runx2这3种蛋白表达量均低于空白组（P<0.05）。Real-time PCR结果显示，人工膜组中BMP2、Smad1、Runx2的mRNA相对表达量与空白组相比，差异均无统计学意义（P＞0.05）。结论 BMP2信号通路在幼龄颅骨缺损修复中起重要作用；人工硬脑膜延长正常颅骨缺损进程。

Abstract:

Objective To investigate the mechanism of cranial defect repair in young animals by analyzing the changes in body weight and the expression of the bone morphogenetic protein 2 （BMP2） signaling pathway during the repair of cranial skull defects in rats.Methods Young Sprague-Dawley rats， aged 10 days， were selected. A bone window with a diameter of about 2 mm was made in the center of the right parietal bone with the sagittal suture of the rat as the boundary， and the bone flap was removed. The rats in the blank group were not given any treatment， and for those in the artificial dura mater group， a 5 mm square artificial dura mater was placed under the defect. The animals were sacrificed and related samples were collected at the end of weeks 2， 4， and 6. There were 6 rats in each group. The two groups were measured in terms of body weight， physiological indicators， and the expression of BMP2， leukocyte suppressor 1 （Smad1）， and Runt-related transcription factor 2 （Runx2） at the site of bone defect.Results Both groups had a reduction in the area of cranial bone defect， and the blank group achieved the repair of 70% of the modeled area at week 4 and the repair of 86% of the modeled area at week 6， while the artificial dura mater group achieved the repair of 20% of the modeled area at week 4 and the repair of 36% of the modeled area at week 6. The artificial dura mater group had significantly lower protein expression levels of BMP2， Smad1， and Runx2 than the blank group at the end of weeks 2， 4， and 6 （P <0.05）， except for BMP2 protein at the end of week 4. Real-time PCR showed that there were no significant differences in the relative mRNA expression levels of BMP2， Smad1， and Runx2 between the artificial dura mater group and the blank group （P >0.05）.Conclusions The BMP2 signaling pathway plays an important role in cranial defect repair in young animals， and artificial dura mater prolongs the process of normal cranial defect repair.