成年大鼠急性压迫性脊髓损伤模型音猬因子的表达

Expression of sonic hedgehog in adult rat models of acute compressive spinal cord injury

背景:在神经系统的发育中,音猬因子信号通路的主要作用为诱导整个中枢神经系统形成背腹两侧分区,当这一信号通路受到破坏时,将导致整个中枢神经系统腹侧表型神经元的完全丧失。目的:制造成年大鼠急性压迫性脊髓损伤模型,检测脊髓急性压迫性损伤后与发育相关的重要分子音猬因子的表达,探讨其在神经再生过程中所发挥的作用。方法:将30只同龄SD大鼠置入后路压迫装置,制作成急性压迫性脊髓损伤模型。随机分为椎板钻孔组5只和急性脊髓损伤组25只。应用原位杂交检测方法,分别于脊髓损伤后1,3,5,7,14 d对损伤区行音猬因子m RNA检测。结果与结论:脊髓损伤后7 d,音猬因子表达水平达到最大值,在损伤区至远端10 mm处的灰质和白质中都有表达。音猬因子在室管膜细胞的表达明显低于在灰质和白质中的表达;其在室管膜区域的表达仅限于损伤区域周围5 mm的范围内,分布范围明显小于在灰质和白质中的表达。提示激活急性压迫性脊髓损伤模型音猬因子的表达,可能和损伤脊髓神经的再生有关。

BACKGROUND：In the development of nervous system, the main effect of sonic hedgehog signaling pathway is to induce the partition of dorsal and ventral sides in the central nervous system. When above signaling pathway is destroyed, ventral neurons in the central nervous system wil completely lose. OBJECTIVE： To establish adult rat models of acute compressive spinal cord injury, to detect the expression of development-related sonic hedgehog after acute compressive spinal cord injury, and to explore its effects on neural regeneration. METHODS：A total of 30 Sprague-Dawley rats at the same age were placed in a posterior compression device to establish models of acute compressive spinal cord injury. They were then randomly divided into lamina driling group （n=5） and acute spinal cord injury group （n=25）. Sonic hedgehog mRNA was detected by in situ hybridization method at the injury site at 1, 3, 5, 7, and 14 days after spinal cord. RESULTS AND CONCLUSION：The expression levels of sonic hedgehog increased to the maximal expression levels in grey and white matters 10 mm distal to the lesion site at 7 days after injury. Sonic hedgehog expression was apparently less in ependymal cels than in grey and white matters and was restricted to 5 mm distal to the lesion site, being narrower in its distribution than its occurrence in grey and white matters. These data indicated that acute compressive spinal cord injury can induce the expression of sonic hedgehog. This expression＆amp;nbsp;maybe relates to adult neural cel regeneration.