CAJ | 학술논문

目的通过对视网膜和视神经神经再生的标志物生长相关蛋白-43( GAP-43)的测定和闪光视觉诱发电位(F-VEP)的测定,观察810 nm低能量镓铝砷(Ga-Al-As)激光对大鼠视神经钳夹伤后视神经再生的影响.方法健康成年W istar大鼠88只,体重(180～ 220)g,分成激光治疗组40只、单纯损伤组32只、正常对照组16只,每组又分成l,3,6,9周4个时间点.标准的视神经钳夹伤模型制备成功后,激光治疗组行激光照射,照射参数为:光导子直径5 mm,照射强度60 mW,持续时间3 min,经皮至视神经损伤处,每日照射1次.单纯损伤组及正常对照组在进行激光照射时,激光器无功率输出.激光治疗l,3,6,9周后测量视网膜、视神经GAP-43mRNA含量和GAP-43蛋白的表达.并且测量损伤前,损伤即刻,治疗1,3,6,9周后患侧眼F-VEP.结果大鼠视神经损伤后,F-VEP有很大变化,表现在N1、P1、N2波潜伏期延长,在视神经损伤即刻,潜伏期瞬间延长,随后有所恢复,第1～3周进行性延长,在第3～9周之间N1、P1、N2波潜伏期有所恢复.激光治疗组N1、Pl、N2波的潜伏期也延长,但是明显小于单纯损伤组.正常的视网膜和视神经中几乎没有GAP-43蛋白的表达,视神经损伤后,GAP-43蛋白的表达在伤后第1周时达到高峰,随后下降,激光治疗后第1,3,6周与同一时间单纯损伤组GAP-43蛋白表达相比有所提高(P＜0.05),视网膜的GAP-43mRNA的含量与GAP-43蛋白表达相一致.结论 810 nm低能量镓铝砷激光能够促进大鼠视神经钳夹伤后视神经再生.
목적 통과대시망막화시신경신경재생적표지물생장상관단백-43( GAP-43)적측정화섬광시각유발전위(F-VEP)적측정,관찰810 nm저능량가려신(Ga-Al-As)격광대대서시신경겸협상후시신경재생적영향.방법 건강성년W istar대서88지,체중(180～ 220)g,분성격광치료조40지、단순손상조32지、정상대조조16지,매조우분성l,3,6,9주4개시간점.표준적시신경겸협상모형제비성공후,격광치료조행격광조사,조사삼수위:광도자직경5 mm,조사강도60 mW,지속시간3 min,경피지시신경손상처,매일조사1차.단순손상조급정상대조조재진행격광조사시,격광기무공솔수출.격광치료l,3,6,9주후측량시망막、시신경GAP-43mRNA함량화GAP-43단백적표체.병차측량손상전,손상즉각,치료1,3,6,9주후환측안F-VEP.결과 대서시신경손상후,F-VEP유흔대변화,표현재N1、P1、N2파잠복기연장,재시신경손상즉각,잠복기순간연장,수후유소회복,제1～3주진행성연장,재제3～9주지간N1、P1、N2파잠복기유소회복.격광치료조N1、Pl、N2파적잠복기야연장,단시명현소우단순손상조.정상적시망막화시신경중궤호몰유GAP-43단백적표체,시신경손상후,GAP-43단백적표체재상후제1주시체도고봉,수후하강,격광치료후제1,3,6주여동일시간단순손상조GAP-43단백표체상비유소제고(P＜0.05),시망막적GAP-43mRNA적함량여GAP-43단백표체상일치.결론 810 nm저능량가려신격광능구촉진대서시신경겸협상후시신경재생.
Objective To determine whether or not 810 nm low power Ga-Al-As laser treatment can stimulate the regeneration of damaged optic nerves by measuring the expression of growth associated protein 43 ( GAP-43 )and flash-visual evoked potential (F-VEP). Methods Eighty-eight Wistar rats weighing (180-220) g were randomly divided into a laser therapy group with 40 rats,an injury group with 32 rats,and a normal control group with 16 rats.Each group was subdivided into 1st,3rd,6th and 9th week subgroups.A standardized crushing of the optic nerve was applied to make the model.After this,the laser therapy group was treated for 3 minutes daily at 60 mW applied transcutaneously to a 5 mm diameter spot on the injured optic nerve.The injury and normal control groups received the same treatment with no laser output.The expression of GAP-43 was detected by immunohistochemistry and RT-PCR after 1,3,6 and 9 weeks of treatment.F-VEP was measured pre-injury,immediately after injury and 1,3,6 and 9 weeks post injury. Results After the optic nerve was injured,obvious changes in F-VEP were detected,including significantly prolonged latencies of N1,P1 and N2 waves.The latency increased immediately after the optic nerve injured,and then recovered,but after 1 and 3 weeks the latency was still prolonged.There was significant recovery from the 3rd to the 9th week.In the laser therapy group,the peak latencies of the N1,P1 and N2 waves were also prolonged,but the changes were less than those in the injury group.Expression of GAP-43 was hardly detectable in normal retinas and optic nerves.GAP-43 had its highest expression level at 1 week post-injury,and then decreased.At the 1st,3rd and 6th week post-injury,the expression of GAP-43 in the laser therapy group was significantly higher than in the injury group.GAP-43 mRNA content in the retina showed the same tendency as GAP-43 protein. Conclusion A 810 nm low power Ga-Al-As laser can promote neural repair and axonal regeneration after optic nerve injury.