睫状神经营养因子对大鼠视神经不全损伤后轴浆运输的影响

目的探讨睫状神经营养因子(CNTF)对大鼠视神经(optic nerve, ON)中度不全损伤后轴浆运输的影响.方法成年雌性Wistar大鼠50只,用无创血管夹于球后1.5 mm钳夹ON 10 s,造成ON中度损伤,于伤后即刻、伤后1、2、4和8周CNTF治疗组玻璃体腔内注射人重组睫状神经营养因子(rhCNTF)2 μg,对照组注射等量双蒸水.分别在不同的时间(1、2、4、8和12周)应用辣根过氧化物酶(horseradish peroxidase, HRP)观察ON不全损伤后顺行轴浆运输的变化.结果伤后1～2周在损伤点后HRP顺染纤维度骤然下降,于上丘均未见HRP显色;伤后4周ON及上丘顺染密度逐渐增强至8周达高峰,对照组ON损伤远端顺染纤维度恢复至正常的12.87%,而治疗组至31.86%.两组间于ON损伤远端和上丘HRP顺染密度均有非常显著性差异(P<0.01).结论 CNTF可改善ON不全损伤后轴浆运输状况,促进ON结构的恢复.

Effects of rhCNTF on axoplasmic transport following incomplete injury of optic nerves of adult rats

Objective To observe the effects of ciliary neurotrophic factor (CNTF) on the recovery of axoplasmic transport following incomplete injury of the optic nerves (ON) of the adult rats. Methods Moderate injury of the optic nerves of 50 adult female rats was induced by crushing the optic nerves for 10 seconds using hemostatic forceps. Recombinant human CNTF (rhCNTF) was injected into the vitreous cavity of CNTF treated group at 0, 1, 2, 4, and 8 weeks after injury. However, the same volume of distilled water was injected into the vitreous cavity of the control rats. The changes of axoplasmic transport were assessed by anterograde labelling combined with horseradish peroxidase (HRP) at 1, 2, 4, 8, and 12 weeks after injury. Results The labelling density at ON distal to the site of injury by HRP obviously decreased at 1 and 2 weeks after injury, and gradually enhanced at 4 weeks and peaked at 8 weeks after injury. The recovery ratios of axoplasmic transport in CNTF treated group and control group at 8 weeks after injury were 31 86% and 12 87%, respectively. No HRP reaction product was observed in the superior colliculus at 1 and 2 weeks after injury. There was significant difference of the HRP anterograde labeling density in ON and the superior colliculus between the CNTF treated group and the control group during 4 to 12 weeks after injury ( P <0.01). Conclusion CNTF can improve the status of axoplasmic transport following incomplete injury of the optic nerves, resulting in the promotion of the recovery of visual functions.