中国实用眼科杂志
中國實用眼科雜誌
중국실용안과잡지
CHINESE JOURNAL OF PRACTICAL OPHTHALMOLOGY
2013年
11期
1482-1487
,共6页
郭小东%胡楚璇%刘洁%刁尧%胡文%王育君%杨虹瑜
郭小東%鬍楚璇%劉潔%刁堯%鬍文%王育君%楊虹瑜
곽소동%호초선%류길%조요%호문%왕육군%양홍유
人参皂Rg1%球周注射%视神经夹伤模型%视网膜组织病理%转录因子Bin-3
人參皂Rg1%毬週註射%視神經夾傷模型%視網膜組織病理%轉錄因子Bin-3
인삼조Rg1%구주주사%시신경협상모형%시망막조직병리%전록인자Bin-3
Ginsenosides Rg1%periocular injection%optic nerve crush model%retinal pathology%transcription factor Brn-3a
目的 研究应用人参皂甙Rg1球周注射对视神经夹伤大鼠组织病理的影响.方法 将SD大鼠随机分成两组,A组12只(24只眼),右眼不做任何处理作为对正常对照组,左眼行视神经夹伤作为损伤对照组.B组12只(24只眼),双眼均行视神经夹伤,右眼注射等体积生理盐水作为治疗对照组,左眼球周注射人参皂甙Rg1(每只眼2 mg/0.1 ml),1次/d,共21 d,作为实验组.用手术显微镜观察各组眼部临床症状学病程变化,用视网膜神经节细胞(RGCs)特异性标记物转录因子Brn-3a标记RGCs,分别于造模成功后3、7、14、28 d进行视网膜组织病理、免疫组织化学染色,比较各组之间差异.结果 (1)视神经钳夹伤3~7 d,损伤组、生理盐水组RGCs单层排列结构消失,组织细胞排列疏松、增厚;实验组视网膜水肿较以上两组程度减轻.(2) 3~28 d各时间点RGCs进行性丢失,细胞数目逐渐减少,晚期阶段视网膜神经节细胞层(GCL)可见空泡化改变;实验组也可见上述改变,但程度较损伤与生理盐水对照组轻.(3)损伤组与生理盐水组RGCs存活数量差异无统计学意义(P>0.05);但实验组RGCs存活数量显著高于同时期生理盐水组对照组,差异具有统计学意义(P<0.05).结论 球周注射人参皂甙Rg1在视神经损伤的病理条件下能够维持眼部与视网膜组织的正常形态结构,提高钳夹伤后RGCs的存活率,减少手术损伤并发症.提示本方法对视神经钳夹伤大鼠的治疗作用安全、有效,有可能用于临床上视神经损伤疾病的治疗.
目的 研究應用人參皂甙Rg1毬週註射對視神經夾傷大鼠組織病理的影響.方法 將SD大鼠隨機分成兩組,A組12隻(24隻眼),右眼不做任何處理作為對正常對照組,左眼行視神經夾傷作為損傷對照組.B組12隻(24隻眼),雙眼均行視神經夾傷,右眼註射等體積生理鹽水作為治療對照組,左眼毬週註射人參皂甙Rg1(每隻眼2 mg/0.1 ml),1次/d,共21 d,作為實驗組.用手術顯微鏡觀察各組眼部臨床癥狀學病程變化,用視網膜神經節細胞(RGCs)特異性標記物轉錄因子Brn-3a標記RGCs,分彆于造模成功後3、7、14、28 d進行視網膜組織病理、免疫組織化學染色,比較各組之間差異.結果 (1)視神經鉗夾傷3~7 d,損傷組、生理鹽水組RGCs單層排列結構消失,組織細胞排列疏鬆、增厚;實驗組視網膜水腫較以上兩組程度減輕.(2) 3~28 d各時間點RGCs進行性丟失,細胞數目逐漸減少,晚期階段視網膜神經節細胞層(GCL)可見空泡化改變;實驗組也可見上述改變,但程度較損傷與生理鹽水對照組輕.(3)損傷組與生理鹽水組RGCs存活數量差異無統計學意義(P>0.05);但實驗組RGCs存活數量顯著高于同時期生理鹽水組對照組,差異具有統計學意義(P<0.05).結論 毬週註射人參皂甙Rg1在視神經損傷的病理條件下能夠維持眼部與視網膜組織的正常形態結構,提高鉗夾傷後RGCs的存活率,減少手術損傷併髮癥.提示本方法對視神經鉗夾傷大鼠的治療作用安全、有效,有可能用于臨床上視神經損傷疾病的治療.
목적 연구응용인삼조대Rg1구주주사대시신경협상대서조직병리적영향.방법 장SD대서수궤분성량조,A조12지(24지안),우안불주임하처리작위대정상대조조,좌안행시신경협상작위손상대조조.B조12지(24지안),쌍안균행시신경협상,우안주사등체적생리염수작위치료대조조,좌안구주주사인삼조대Rg1(매지안2 mg/0.1 ml),1차/d,공21 d,작위실험조.용수술현미경관찰각조안부림상증상학병정변화,용시망막신경절세포(RGCs)특이성표기물전록인자Brn-3a표기RGCs,분별우조모성공후3、7、14、28 d진행시망막조직병리、면역조직화학염색,비교각조지간차이.결과 (1)시신경겸협상3~7 d,손상조、생리염수조RGCs단층배렬결구소실,조직세포배렬소송、증후;실험조시망막수종교이상량조정도감경.(2) 3~28 d각시간점RGCs진행성주실,세포수목축점감소,만기계단시망막신경절세포층(GCL)가견공포화개변;실험조야가견상술개변,단정도교손상여생리염수대조조경.(3)손상조여생리염수조RGCs존활수량차이무통계학의의(P>0.05);단실험조RGCs존활수량현저고우동시기생리염수조대조조,차이구유통계학의의(P<0.05).결론 구주주사인삼조대Rg1재시신경손상적병리조건하능구유지안부여시망막조직적정상형태결구,제고겸협상후RGCs적존활솔,감소수술손상병발증.제시본방법대시신경겸협상대서적치료작용안전、유효,유가능용우림상상시신경손상질병적치료.
Objective To make a study on the histopathological influence of ginsenosides Rg1 periocular injection after optic nerve crush in rats.Method SD rats were randomly divided into two groups,A group of 12 (24 eyes),the right eye without any treatment as a normal control group,left eye made optic nerve crush as the control group.Group B,12 (24 eyes),eyes underwent optic nerve crush,right eye injected with saline as a treatment control group,the left eye injected with ginsenosides Rg1 (2mg/0.1ml / eyes) as the experimental group.Clinical symptomatology changes of each group were observed with a surgical microscope,specific markers transcription factor Brn-3a labeled retinal ganglion cells (RGCs),pathology and immunohistochemistry were examined at 3,7,14,28 d after injury,respectively.Differences between groups were compared.Results (1) at 3-7d after optic crush,monolayer structure of injury and saline group disappeared,tissue loosely arranged thickening,retinal edema of the experimental group lessened compared with that of the two sets.(2)progressive loss of RGCs were observed at 3~28d,the number of cells reduced gradually,vacuoles appeared at the late stage.These changes were also seen in experimental group and degree of injury was lighter than those of two groups.(3)There was no significant difference between the survival in injury and saline group (P >0.05); survival number of RGCs in experimental group was significantly higher than that of saline control group,the difference was statistically significant(P <0.05).Conclusions Rg1 ginsenosides Rg1 periocular injection can maintain the normal morphology structure of optic retinal tissue,improve the survival rate after nerve crush damage.It hints that this method is safe,effective and may be used in clinical optic nerve diseases.