药学与临床研究
藥學與臨床研究
약학여림상연구
PHARMACEUTICAL AND CLINICAL RESEARCH
2015年
2期
107-111
,共5页
高晨%荔志云%贾平%张景科
高晨%荔誌雲%賈平%張景科
고신%려지운%가평%장경과
依达拉奉%颅眶联合伤%视神经%活性氧%凋亡
依達拉奉%顱眶聯閤傷%視神經%活性氧%凋亡
의체랍봉%로광연합상%시신경%활성양%조망
Edaravone%Cranio-orbital injury%Retinal ganglion cells%Reactive oxygen species%Apoptosis
目的：探讨实验性大鼠颅眶联合损伤（cranio-orbital injury，COI）后视神经损伤机制及依达拉奉的保护作用。方法：144只清洁级SD大鼠，雌雄各半，随机分为对照组、损伤组和治疗组，每组48只。损伤组和治疗组大鼠利用液压冲击颅脑损伤仪建立颅眶联合伤模型，治疗组造模以后腹腔注射依达拉奉30 mg·kg-1，每日2次，共14日。3组分别在造模后3、6、10、14 d取视网膜组织，检测视网膜神经节细胞（retinal ganglion cells，RGCs）活性氧（reactive oxygen species， ROS）含量及不同时间点RGCs凋亡率，光镜下观察视网膜HE染色微观结构，共聚焦显微镜下观察RGCs的TUNEL荧光标记凋亡情况。结果：造模后损伤组RGCs的ROS含量逐渐升高，第10天达到高峰，RGCs凋亡率变化趋势与此相一致，与对照组及治疗组差异有统计学意义（P＜0.05），治疗组与对照组相比较无明显差异。光镜下损伤组视网膜结构紊乱，损伤组RGCs的TUNEL荧光标记阳性率明显高于其余两组。结论：COI后RGCs的ROS含量明显升高，导致细胞出现凋亡失调。依达拉奉通过清除ROS逆转这一病理过程，具有明确的视神经保护作用，值得临床推广。
目的：探討實驗性大鼠顱眶聯閤損傷（cranio-orbital injury，COI）後視神經損傷機製及依達拉奉的保護作用。方法：144隻清潔級SD大鼠，雌雄各半，隨機分為對照組、損傷組和治療組，每組48隻。損傷組和治療組大鼠利用液壓遲擊顱腦損傷儀建立顱眶聯閤傷模型，治療組造模以後腹腔註射依達拉奉30 mg·kg-1，每日2次，共14日。3組分彆在造模後3、6、10、14 d取視網膜組織，檢測視網膜神經節細胞（retinal ganglion cells，RGCs）活性氧（reactive oxygen species， ROS）含量及不同時間點RGCs凋亡率，光鏡下觀察視網膜HE染色微觀結構，共聚焦顯微鏡下觀察RGCs的TUNEL熒光標記凋亡情況。結果：造模後損傷組RGCs的ROS含量逐漸升高，第10天達到高峰，RGCs凋亡率變化趨勢與此相一緻，與對照組及治療組差異有統計學意義（P＜0.05），治療組與對照組相比較無明顯差異。光鏡下損傷組視網膜結構紊亂，損傷組RGCs的TUNEL熒光標記暘性率明顯高于其餘兩組。結論：COI後RGCs的ROS含量明顯升高，導緻細胞齣現凋亡失調。依達拉奉通過清除ROS逆轉這一病理過程，具有明確的視神經保護作用，值得臨床推廣。
목적：탐토실험성대서로광연합손상（cranio-orbital injury，COI）후시신경손상궤제급의체랍봉적보호작용。방법：144지청길급SD대서，자웅각반，수궤분위대조조、손상조화치료조，매조48지。손상조화치료조대서이용액압충격로뇌손상의건립로광연합상모형，치료조조모이후복강주사의체랍봉30 mg·kg-1，매일2차，공14일。3조분별재조모후3、6、10、14 d취시망막조직，검측시망막신경절세포（retinal ganglion cells，RGCs）활성양（reactive oxygen species， ROS）함량급불동시간점RGCs조망솔，광경하관찰시망막HE염색미관결구，공취초현미경하관찰RGCs적TUNEL형광표기조망정황。결과：조모후손상조RGCs적ROS함량축점승고，제10천체도고봉，RGCs조망솔변화추세여차상일치，여대조조급치료조차이유통계학의의（P＜0.05），치료조여대조조상비교무명현차이。광경하손상조시망막결구문란，손상조RGCs적TUNEL형광표기양성솔명현고우기여량조。결론：COI후RGCs적ROS함량명현승고，도치세포출현조망실조。의체랍봉통과청제ROS역전저일병리과정，구유명학적시신경보호작용，치득림상추엄。
Objective: To investigate the mechanism of optic nerve injury and protective effects of edar-avone on rats with experimental cranio-orbital injury (COI). Methods: A total of 144 rats (clean grade) were randomly divided into control group, injury group and treatment group, with 48 rats in each group. The animal model of COI was established in the left eyes of rats of injury and treatment groups by a fluid percussion brain injury (FPI) device. Edaravone (30 mg·kg-1) diluted with normal saline was injected in-traperitoneally to the rats of treatment group after modeling every 12 hours for 14 days. Rat retina was ob-tained at 3, 6, 10 and 14 day, respectively, after injury, to check the content of reactive oxygen species (ROS) in retinal ganglion cells (RGCs) and the apoptosis rate of RGCs. The HE stained microstructure of RGCs was observed under an optical microscope. The TUNEL fluorescence labeled apoptosis of RGCs was observed under a laser confocal microscope. Results: The content of ROS as well as the apoptosis rate of RGCs increased gradually and reached maximum in 10 days after modeling in the injury group. There were statistically significant differences between the injury group and the other two groups (P<0.05). The retina structure of the injury group was disorganized after injury. The positive rate of TUNEL fluorescence labeled RGCs in the injury group was significantly higher than the other two groups. Conclusion: The content of ROS in RGCs increased significantly after COI, resulted in apoptosis imbalance of RGCs. Edaravone pre-vents this pathological process by eliminating ROS and thus has a protective effect on optic nerve, which is worthy of clinical promotion.
