摘要
为了探讨大鼠坐骨神经损伤对CDK11P58和Cyclin D3表达的影响,本实验将成年SD大鼠随机分为假手术组和夹伤组,运用Western blot结合免疫荧光组织化学双标技术,观察了坐骨神经损伤后坐骨神经夹伤段、脊髓腰膨大前角和伤侧腓肠肌内CDK11P58和Cyclin D3的表达变化。结果显示:(1)坐骨神经夹伤后,坐骨神经夹伤段及脊髓腰膨大前角、伤侧腓肠肌中的CDK11P58蛋白的表达先逐渐下降,后又逐渐上升;而Cyclin D3的表达无明显变化;(2)在假手术组的坐骨神经、脊髓腰膨大前角和腓肠肌内都可观察到CDK11P58和Cyclin D3的表达;而坐骨神经夹伤后,在上述部位可检测到CDK11P58的表达强度明显减弱,但Cyclin D3无明显变化;(3)免疫荧光双标结果显示CDK11P58和Cyclin D3在假手术组的坐骨神经、脊髓腰膨大前角和伤侧腓肠肌内都有共存;而在坐骨神经损伤后这种共存强度明显降低。以上结果提示,坐骨神经损伤可影响坐骨神经及脊髓腰膨大、伤侧腓肠肌内CDK11P58的表达,但对Cyclin D3无明显影响,表明CDK11P58可能在周围神经损伤和修复中发挥重要作用。
To investigate the effects of sciatic nerve injury on the expression of CDKll^p58and Cyclin D3, the adult rats were randomly divided into sham group and sciatic nerve crushed group in the present study. By Western blot and double-immunofluorescence histochemical technique, we observed the expression changes of CDKll^p58 and Cyclin D3 in the injured sciatic nerve, the anterior horn of spinal intumescentia lumbalis and gastroenemius after sciatic nerve crush. The results showed that: ( 1 ) Expressions of CDKll^p58 were detected in the injured sciatic nerve, the anterior horn of spinal intumescentia lumbalis and gastroenemius, and the expression levels of CDKll^p58 were gradually declined after sciatic nerve crush, then it was gradually rescued; but the expression of Cyclin D3 was no obvious changes; (2) Expressions of CDKll^p58 and Cyclin D3 were observed in the sciatic nerve, spinal intumescentia lumbalis and gastrocnemius in the sham group After sciatic nerve crush, the immunofluorescence densities of CDK11 ess were declined in above regions, however, the fluorescence densities of CyclinD3 were constant; (3) The results of double-labeled indicated that CDKll^p58 and Cyclin D3 coexisted in the sciatic nerve, the spinal intumescentia lumbalis and gastrocnemius, however, the coexistence reduced after sciatic nerve crush. These results indicate that sciatic nerve lesion can affect the expression of CDKll^p58 in the sciatic nerve, the spinal intumescentia lumbalis and gastroenemius, but the expression of Cyclin D3 was no obvious influence, which suggest CDKll^p58 may play an important role in the damage and reparation of peripheral nerve.
出处
《神经解剖学杂志》
CAS
CSCD
北大核心
2007年第5期542-548,共7页
Chinese Journal of Neuroanatomy
基金
国家自然科学基金(Nos30300099
30770488)
江苏省自然科学基金(NoBK2003035)
江苏省高校自然科学研究项目(Nos03KJB180109
04KJB320114)
江苏省社会发展科技指导性计划项目(NoBS2004526)
江苏省"六大人才高峰"第二批资助项目