中华眼外伤职业眼病杂志
中華眼外傷職業眼病雜誌
중화안외상직업안병잡지
CHINESE JOURNAL OF OCULAR TRAUMA AND OCCUPATIONAL EYE DISEASE
2013年
10期
726-730
,共5页
张俊琦%胡丽荣%邢达勇%刘志英%刘太平
張俊琦%鬍麗榮%邢達勇%劉誌英%劉太平
장준기%호려영%형체용%류지영%류태평
视神经夹伤%视网膜%一氧化氮%凋亡%氨基胍
視神經夾傷%視網膜%一氧化氮%凋亡%氨基胍
시신경협상%시망막%일양화담%조망%안기고
Optic nerve crush%Retina%Nitric oxide%Apoptosis%Aminoguanidine
目的 通过建立兔视神经夹伤模型,观察伤后视网膜组织中一氧化氮的表达与视网膜神经节细胞(RGCs)凋亡的关系,从而探讨RGCs凋亡机制及氨基胍(AG)在伤后对RGCs的保护性作用.方法 55只成年大耳白兔,随机分正常对照组(5只)、损伤对照组(25只)、AG治疗组(25只).损伤组双眼夹伤视神经,按伤后1、3、7、14、21 d又随机分为5组(5只/组).AG治疗组于伤后2 min耳缘静脉注射2％ AG,损伤对照组同法注射生理盐水.应用TUNEL染色计数凋亡阳性细胞;比色法测量一氧化氮(NO)含量、诱导型一氧化氮合酶(iNOS)活力.结果 正常组视网膜切片中极少见RGCs凋亡.损伤组于伤后1d偶见,3～7d逐渐增多,至14 d达高峰,之后逐渐下降.正常视网膜组织中很少表达iNOS,但含有少量NO.在损伤后二者含量逐渐增高,与RGCs凋亡呈正相关性.同一时间点损伤对照组和AG治疗组比较差异有统计学意义.结论 兔视神经夹伤后,NO合成增多可能是引起RGCs凋亡的一个因素.而AG通过减少NO的合成,降低RGCs凋亡,对RGCs有保护性作用.
目的 通過建立兔視神經夾傷模型,觀察傷後視網膜組織中一氧化氮的錶達與視網膜神經節細胞(RGCs)凋亡的關繫,從而探討RGCs凋亡機製及氨基胍(AG)在傷後對RGCs的保護性作用.方法 55隻成年大耳白兔,隨機分正常對照組(5隻)、損傷對照組(25隻)、AG治療組(25隻).損傷組雙眼夾傷視神經,按傷後1、3、7、14、21 d又隨機分為5組(5隻/組).AG治療組于傷後2 min耳緣靜脈註射2％ AG,損傷對照組同法註射生理鹽水.應用TUNEL染色計數凋亡暘性細胞;比色法測量一氧化氮(NO)含量、誘導型一氧化氮閤酶(iNOS)活力.結果 正常組視網膜切片中極少見RGCs凋亡.損傷組于傷後1d偶見,3～7d逐漸增多,至14 d達高峰,之後逐漸下降.正常視網膜組織中很少錶達iNOS,但含有少量NO.在損傷後二者含量逐漸增高,與RGCs凋亡呈正相關性.同一時間點損傷對照組和AG治療組比較差異有統計學意義.結論 兔視神經夾傷後,NO閤成增多可能是引起RGCs凋亡的一箇因素.而AG通過減少NO的閤成,降低RGCs凋亡,對RGCs有保護性作用.
목적 통과건립토시신경협상모형,관찰상후시망막조직중일양화담적표체여시망막신경절세포(RGCs)조망적관계,종이탐토RGCs조망궤제급안기고(AG)재상후대RGCs적보호성작용.방법 55지성년대이백토,수궤분정상대조조(5지)、손상대조조(25지)、AG치료조(25지).손상조쌍안협상시신경,안상후1、3、7、14、21 d우수궤분위5조(5지/조).AG치료조우상후2 min이연정맥주사2％ AG,손상대조조동법주사생리염수.응용TUNEL염색계수조망양성세포;비색법측량일양화담(NO)함량、유도형일양화담합매(iNOS)활력.결과 정상조시망막절편중겁소견RGCs조망.손상조우상후1d우견,3～7d축점증다,지14 d체고봉,지후축점하강.정상시망막조직중흔소표체iNOS,단함유소량NO.재손상후이자함량축점증고,여RGCs조망정정상관성.동일시간점손상대조조화AG치료조비교차이유통계학의의.결론 토시신경협상후,NO합성증다가능시인기RGCs조망적일개인소.이AG통과감소NO적합성,강저RGCs조망,대RGCs유보호성작용.
Objective Through establishing the model of optic nerve crush in rabbits,to observe expression of nitric oxide (NO) in retinal tissue and apoptosis of retinal ganglion cells after trauma,to investigate the apoptosis mechanism of RGCs and protective effect of Aminoguanidine (AG) to RGCs after injury.Methods Fifty-five adult rabbits were randomly divided into normal control group (n =5),injury control group (n =25) and AG treatment group (n =25).The optic nerve of both eyes were crushed in injury group,According to 1 d、3 d、7 d、14 d and 21 d after injury,the injury group were divided into 5 subgroups (n =5).AG treatment group were injected 2％ AG through ear-border vein 2 min after injury.The injury control group were injected equal volume of NS through ear-border vein.Retinal slice stained TUNEL was selected to locate and calculate apoptosis cells.NO content and inducible nitric oxide synthase (iNOS) vitality were determined with biochemistry method.Results Few apoptosis cells were detected at normal retina.A few apoptosis cells were detected in 1d after injury,there were a significant number of TUNEL positive cells in 3 ～ 7d after injury,The number of TUNEL positive cells reached a maximum in 14 d after injury,followed by a decrease.iNOS was expressed rarely in normal retinal tissue,but it contains a small amount of NO.Both content increased gradually after injury,the expression of NO and iNOS were positive correlated with apoptosis of RGCs.The injury in treatment group and the injury in control group were significantly different (P ＜ 0.05) at the same time point.Conclusion The experiment show that the increase of NO synthesis may be a factor apoptosis of RGCs after optic nerve crush in rabbits.AG can reduce NO synthesis,reduce the degree of apoptosis of RGCs,and protect the RGCs after optic nerve injury.
