CAJ | 학술논문

目的探讨睫状神经营养因子(CNTF)玻璃体内注射对鼠慢性青光眼视神经的保护作用.方法通过散瞳、前房穿刺放液及角膜缘激光光凝等步骤制造鼠慢性青光眼模型.设正常对照组、前房穿刺对照组、未治疗组(仅造模)、治疗组(造模后双眼玻璃体内注入CNTF)、治疗对照组(造模后双眼玻璃体内注入生理盐水).观察视网膜组织磷酸化信号转导与转录激活子3(pSTAT3)表达、视神经轴突及闪光视觉诱发电位(F-VEP)变化.结果正常状态pSTAT3在视网膜组织中极少表达,眼压升高后1 d开始上升,2 d达到高峰,14 d下降到正常水平.治疗组视网膜中pSTAT3在眼压升高14 d和28 d表达均高于同时问段的未治疗组及治疗对照组(P＜0.05).在眼压升高28 d治疗组视神经纤维阳性面积比率的值明显高于未治疗组及治疗对照组,且VEPP1波潜伏期明显低于以上两组(P＜0.05).结论 CNTF玻璃体内注射延缓了鼠慢性青光眼视神经的损伤.眼压升高初期,视网膜STAT3信号传导途径暂时被激活,CNTF相对长时间激活了STAT3信号传导途径,STATB信号传导途径参与介导了CNTF对视神经的保护作用.
목적 탐토첩상신경영양인자(CNTF)파리체내주사대서만성청광안시신경적보호작용.방법 통과산동、전방천자방액급각막연격광광응등보취제조서만성청광안모형.설정상대조조、전방천자대조조、미치료조(부조모)、치료조(조모후쌍안파리체내주입CNTF)、치료대조조(조모후쌍안파리체내주입생리염수).관찰시망막조직린산화신호전도여전록격활자3(pSTAT3)표체、시신경축돌급섬광시각유발전위(F-VEP)변화.결과 정상상태pSTAT3재시망막조직중겁소표체,안압승고후1 d개시상승,2 d체도고봉,14 d하강도정상수평.치료조시망막중pSTAT3재안압승고14 d화28 d표체균고우동시문단적미치료조급치료대조조(P＜0.05).재안압승고28 d치료조시신경섬유양성면적비솔적치명현고우미치료조급치료대조조,차VEPP1파잠복기명현저우이상량조(P＜0.05).결론 CNTF파리체내주사연완료서만성청광안시신경적손상.안압승고초기,시망막STAT3신호전도도경잠시피격활,CNTF상대장시간격활료STAT3신호전도도경,STATB신호전도도경삼여개도료CNTF대시신경적보호작용.
Objective To investigate the neuroprotective function of ciliary neurotrophic factor (CNTF)intravitreal injection in the model of chronic glaucoma in rats.Methods SD rats were used to develop chronic glaucoma model.First,pupil dilation;Second,the anterior chamber was flattened by aspiration of aqueous humor;Third,laser photecoagulation Was performed to the limbus.Groups:Normal control group、Aterior chamber flattened group、Non-treatment group、Treatment group(CNTF intravitreal injection)、Treatment control group(0.9%sodium chloride injection intravitreal injection).Expression of phosphorylated signal transdueer and activator of transcription(sSTAT3)in the retinal tissue、optic nerve axons and flash visual evoked potential(F-VEP)in different periods were observed.Results There Was little expression of pSTAT3 in the normal retina.The expression of sSTAT3 increased in the first day of IOP being elevated in the non-treatment group,which reached its maximum in the second day and dropped to normal levels in the 14th day.In the CNTF treatment group,the expression of pSTAT3 Was still higher in the 14th and 28th day of IOP being elevated than that in the non-treat ment group and treatment control group.At the end of this study (28 d)the rate of positive area ofoptic nerve fibre in the treatment group was signifcanfly higher than that in the non-treatment group and treatment control group(P＜0.05).The latency time of F-VEP in the non-treatment group was significantly prolonged,which was longer than that in the treatment group(P＜0.05).Conclusion CNTF intravitreal injection has protective effect on the retinal tissue in the model of chronic glaucoma in rats,which relieves the trauma of optic nerve.During the early stage of chronic glaucoma,STAT3 pathway was activated temporarily.CNTF induced the comparatively long period activated of STAT3 pathway.STAT3 pathway,as one of the signal pathways of CNTF,took part in the the neuroprotective function of CNTF.