CAJ | 학술논문

目的在体外研究人参皂苷Rb1（ GRb1）对谷氨酸漏出所导致海马神经元损伤的保护作用，并探讨可能的作用机制。方法培养至10 d的海马神经元分为谷氨酸损伤组和GRb1治疗组，以MTT法测定细胞存活率，以Hoechst 33258染色法检测细胞凋亡，丙二醛（ MDA）、超氧化物歧化酶（ SOD）测定细胞氧化损伤程度。结果与正常对照组比较，谷氨酸（1.25、2.5、5、10μmol/L ）作用2 h后细胞活力下降，分别为（93.9±2.1）％、（82.3±1.4）％、（51.2±1.2）％、（32.7±1.3）％。其中谷氨酸5μmol/L作用2 h后存活（51.2±1.2）％的细胞（与对照组比较，P＜0.01），接近对照组的50％。与对照组相比，给予5μmol/L谷氨酸作用2 h后，谷氨酸组脂质过氧化产物MDA水平上升[（7.52±0.11）nmol/mg pro vs．（3.93±0.36）nmol/mg pro]；抗氧化的SOD活性明显下降[（37.28±1.72）NU/mg pro vs．（55.39±1.73）NU/mg pro]。同时观察到大量的凋亡细胞出现[（34.5±1.8）％，与对照组比较，P＜0.01]。而与谷氨酸组（5μmol/L，2 h）相比， GRb1（1、10、100、200μmol/L）能够明显提高细胞存活率，分别是（64.9±1.7）％、（72.3±2.2）％、（70.4±3.2）％、（71.6±2.3）％，P＜0.01，GRb11、10、100μmol/L组可以观察到MDA水平的轻度下降，但与谷氨酸组比较没有统计学差异，GRb110、100μmol/L可以提高SOD活性（ P＜0.01），GRb11μmol/L组未观察到该效应。给予GRb11、10、100μmol/L 干预后细胞凋亡率下降，分别为（27.3±1.7）％、（19.4±1.2）％、（23.5±1.9）％，P＜0.01。结论 GRb1具有良好的神经保护作用，其保护作用与抗氧化及抗凋亡有关。
목적재체외연구인삼조감Rb1（ GRb1）대곡안산루출소도치해마신경원손상적보호작용，병탐토가능적작용궤제。방법배양지10 d적해마신경원분위곡안산손상조화GRb1치료조，이MTT법측정세포존활솔，이Hoechst 33258염색법검측세포조망，병이철（ MDA）、초양화물기화매（ SOD）측정세포양화손상정도。결과여정상대조조비교，곡안산（1.25、2.5、5、10μmol/L ）작용2 h후세포활력하강，분별위（93.9±2.1）％、（82.3±1.4）％、（51.2±1.2）％、（32.7±1.3）％。기중곡안산5μmol/L작용2 h후존활（51.2±1.2）％적세포（여대조조비교，P＜0.01），접근대조조적50％。여대조조상비，급여5μmol/L곡안산작용2 h후，곡안산조지질과양화산물MDA수평상승[（7.52±0.11）nmol/mg pro vs．（3.93±0.36）nmol/mg pro]；항양화적SOD활성명현하강[（37.28±1.72）NU/mg pro vs．（55.39±1.73）NU/mg pro]。동시관찰도대량적조망세포출현[（34.5±1.8）％，여대조조비교，P＜0.01]。이여곡안산조（5μmol/L，2 h）상비， GRb1（1、10、100、200μmol/L）능구명현제고세포존활솔，분별시（64.9±1.7）％、（72.3±2.2）％、（70.4±3.2）％、（71.6±2.3）％，P＜0.01，GRb11、10、100μmol/L조가이관찰도MDA수평적경도하강，단여곡안산조비교몰유통계학차이，GRb110、100μmol/L가이제고SOD활성（ P＜0.01），GRb11μmol/L조미관찰도해효응。급여GRb11、10、100μmol/L 간예후세포조망솔하강，분별위（27.3±1.7）％、（19.4±1.2）％、（23.5±1.9）％，P＜0.01。결론 GRb1구유량호적신경보호작용，기보호작용여항양화급항조망유관。
Objective To investigate the neuroprotective effect of ginsenoside Rb 1 ( GRb1 ) on glutamate induced hippocampal neurons injury and the possible mechanisms .Methods Hippocampal neurons cultured for 10 days was divided into glutamate treated group and GRb 1 treated group .MTT method was used to test the cell viability,Hoechst 33258 was used to detect the cell apoptosis , MDA, SOD method were adopt to determine the oxidative damage.Results To compared with control group,glutamate(1.25,2.5,5,10 μmol/L;2 h)group cell viability was decline ,respectively ( 93.9 ±2.1 )%;( 82.3 ±1.4 )%;( 51.2 ±1.2 )%;( 32.7 ±1.3 )%.After 5μmol/L glutamate treated for 2 h,cell viability declined to(51.2 ±1.2)%(P<0.01 vs.control group),nearly 50%of the control group .And MDA level was increased compared with control group [ ( 7.52 ±0.11 ) nmol/mg pro vs. (3.93 ±0.36)nmol/mg pro];SOD level had significant decline [(37.28 ±1.72)NU/mg pro vs.(55.39 ±1.73) NU/mg pro].Meanwhile,cell apoptosis was increased significantly [(34.5 ±1.8)%,P<0.01 vs.control group]. Compared with glutamate(5 μmol/L,2 h)treated group,GRb1(1,10,100,200 μmol/L)could increase cell viability (64.9 ±1.7)%,(72.3 ±2.2)%,(70.4 ±3.2)%,(71.6 ±2.3)%,P<0.01 vs.glutamate-treated group,GRb1 1,10,100 μmol/L treated group had slightly decreased MDA level ,but had no significant difference with glutamate treated group.GRb1 10,100 μmol/L could increase the SOD activity(P<0.01 vs.glutamate-treated group),GRb1 1 μmol/L group did not have this effect .Cell apoptosis rate was decline when treated with 1,10,100 μmol/L GRb1, respectively( 27.3 ±1.7 )%, ( 19.4 ±1.2 )%, ( 23.5 ±1.9 )%, P <0.01 vs.glutamate-treated group. Conclusions GRb1 could confront glutamate induced neurons injury ,the neuroprotective effect was related to anti- oxidation and reducing apoptosis .