卒中与神经疾病
卒中與神經疾病
졸중여신경질병
2015年
4期
203-206
,共4页
脑缺血%人参皂甙%再灌注损伤%Rb1%NgR
腦缺血%人參皂甙%再灌註損傷%Rb1%NgR
뇌결혈%인삼조대%재관주손상%Rb1%NgR
Cerebral ischemia%Ginseng%Rb1%Reperfusion injury%NgR
目的：观察人参皂甙单体 Rb1对大鼠实验性脑缺血的保护作用。方法健康成年雄性清洁级SD 大鼠随机分为假手术组(Sham)、缺血对照组(Con)、干预组(Tre),干预组又分为 Rb130 mg/kg、60 mg/kg及90 mg/kg 三个不同剂量组。缺血对照组采用线栓法建立大脑中动脉闭塞模型,缺血2 h后拨出线栓再灌注；各干预组用相应剂量 Rb1 ip qd×7 d,末次给药后3 h内用同样方法建立大脑中动脉闭塞模型及再灌注；假手术组不插入线栓,余操作相同。术后48 h取标本 TTC 染色测梗死体积、干湿重法脑组织含水量测定、Tun-nel 法测定调亡细胞数及 NgR 表达的免疫组化测定。结果各干预组的梗死体积分别为30 mg/kg组(27.629±1.401)%,60 mg/kg 组(24.164± 1.710)%,90mg/kg 组(21.955±2.556)%,缺血对照组为(29.846 ± 1.153)%；脑组织含水量为30 mg/kg组(80.079±0.726)%,60 mg/kg 组(78.984±0.902)%,90 mg/kg 组(77.855±0.258)%,假手术组与缺血对照组分别为(76.517±0.37)%、(81.799±1.065)%；调亡细胞数分别为30 mg/kg 组(89.000±10.296),60 mg/kg 组(59.000±12.522),90 mg/kg 组(36.667±19.054),假手术组与缺血对照组分别为(1.600± 1.517)、(132.667±22.223)；NgR 表达阳性面积分别为30 mg/kg 组(84.827±3.870),90 mg/kg 组(66.040±5.541),60 mg/kg 组(75.577± 7.150),假手术组与缺血对照组分别为(48.355±9.720)、(91.485±5.822)。结论人参皂甙单体 Rb1对大鼠实验性脑缺血有保护作用,能减轻缺血再灌注损伤所致的脑水肿及梗塞面积,减少细胞调亡,并且该保护作用呈剂量依赖性。对 NgR 表达的干预提示 Rb1可能在脑缺血死后神经可塑性中起促进作用。
目的：觀察人參皂甙單體 Rb1對大鼠實驗性腦缺血的保護作用。方法健康成年雄性清潔級SD 大鼠隨機分為假手術組(Sham)、缺血對照組(Con)、榦預組(Tre),榦預組又分為 Rb130 mg/kg、60 mg/kg及90 mg/kg 三箇不同劑量組。缺血對照組採用線栓法建立大腦中動脈閉塞模型,缺血2 h後撥齣線栓再灌註；各榦預組用相應劑量 Rb1 ip qd×7 d,末次給藥後3 h內用同樣方法建立大腦中動脈閉塞模型及再灌註；假手術組不插入線栓,餘操作相同。術後48 h取標本 TTC 染色測梗死體積、榦濕重法腦組織含水量測定、Tun-nel 法測定調亡細胞數及 NgR 錶達的免疫組化測定。結果各榦預組的梗死體積分彆為30 mg/kg組(27.629±1.401)%,60 mg/kg 組(24.164± 1.710)%,90mg/kg 組(21.955±2.556)%,缺血對照組為(29.846 ± 1.153)%；腦組織含水量為30 mg/kg組(80.079±0.726)%,60 mg/kg 組(78.984±0.902)%,90 mg/kg 組(77.855±0.258)%,假手術組與缺血對照組分彆為(76.517±0.37)%、(81.799±1.065)%；調亡細胞數分彆為30 mg/kg 組(89.000±10.296),60 mg/kg 組(59.000±12.522),90 mg/kg 組(36.667±19.054),假手術組與缺血對照組分彆為(1.600± 1.517)、(132.667±22.223)；NgR 錶達暘性麵積分彆為30 mg/kg 組(84.827±3.870),90 mg/kg 組(66.040±5.541),60 mg/kg 組(75.577± 7.150),假手術組與缺血對照組分彆為(48.355±9.720)、(91.485±5.822)。結論人參皂甙單體 Rb1對大鼠實驗性腦缺血有保護作用,能減輕缺血再灌註損傷所緻的腦水腫及梗塞麵積,減少細胞調亡,併且該保護作用呈劑量依賴性。對 NgR 錶達的榦預提示 Rb1可能在腦缺血死後神經可塑性中起促進作用。
목적：관찰인삼조대단체 Rb1대대서실험성뇌결혈적보호작용。방법건강성년웅성청길급SD 대서수궤분위가수술조(Sham)、결혈대조조(Con)、간예조(Tre),간예조우분위 Rb130 mg/kg、60 mg/kg급90 mg/kg 삼개불동제량조。결혈대조조채용선전법건립대뇌중동맥폐새모형,결혈2 h후발출선전재관주；각간예조용상응제량 Rb1 ip qd×7 d,말차급약후3 h내용동양방법건립대뇌중동맥폐새모형급재관주；가수술조불삽입선전,여조작상동。술후48 h취표본 TTC 염색측경사체적、간습중법뇌조직함수량측정、Tun-nel 법측정조망세포수급 NgR 표체적면역조화측정。결과각간예조적경사체적분별위30 mg/kg조(27.629±1.401)%,60 mg/kg 조(24.164± 1.710)%,90mg/kg 조(21.955±2.556)%,결혈대조조위(29.846 ± 1.153)%；뇌조직함수량위30 mg/kg조(80.079±0.726)%,60 mg/kg 조(78.984±0.902)%,90 mg/kg 조(77.855±0.258)%,가수술조여결혈대조조분별위(76.517±0.37)%、(81.799±1.065)%；조망세포수분별위30 mg/kg 조(89.000±10.296),60 mg/kg 조(59.000±12.522),90 mg/kg 조(36.667±19.054),가수술조여결혈대조조분별위(1.600± 1.517)、(132.667±22.223)；NgR 표체양성면적분별위30 mg/kg 조(84.827±3.870),90 mg/kg 조(66.040±5.541),60 mg/kg 조(75.577± 7.150),가수술조여결혈대조조분별위(48.355±9.720)、(91.485±5.822)。결론인삼조대단체 Rb1대대서실험성뇌결혈유보호작용,능감경결혈재관주손상소치적뇌수종급경새면적,감소세포조망,병차해보호작용정제량의뢰성。대 NgR 표체적간예제시 Rb1가능재뇌결혈사후신경가소성중기촉진작용。
Objective To observe the protection of ginseng Rb1 in rats with local cerebral ischemic reperfusion injury.Methods Healthy Sprague-Dawley rats were divided into three groups:Sham,control and treat group.Treat group was divided into three subgroups :Rb1 30 mg/kg、60 mg/kg and 90 mg/kg group. MCAO models were created after seven days of Rb1 ip qd in treat group with respective dose and NS ip qd in control group.Tthe line extracted after occlusion 2 h.Sham group only receives sham operation.Rats were sacrificed at 48 h.The markers such as the expression intensity of NgR protein,brain water content,volume of infarction by TTC staining,and the count of apoptosis cell were estimated.Results Compared with control groups,the levels of expression of NgR protein,brain water content,volume of infarction and the count of ap-optosis cell were lower in treat group and showed statistical difference (P <0.05).In treat group,there was also statistical difference between three subgroups.Conclusions The article show ginseng Rb1 has protective effect on rats with local cerebral ischemic reperfusion injury.Rb1 can decrease brain edema,infarction volume and apoptosis cell counting induced by local ischemic perfusion injury.It also indicates Rb1 may play a role in rehabilitation after CNS injury because Rb1 reduced the expression of NgR protein.
