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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Rb1ip 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、Tunnel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。
Objective To observe the protective effect of ginsenoside Rb1 on experimental cerebral ischemia in rats. Methods Healthy adult male SD rats were randomly divided into sham group, ischemia control group and intervention group. The intervention group was divided into Rb130 mg / kg, 60 mg / kg and 90 mg / kg three different dose groups. In the ischemic control group, the middle cerebral artery occlusion model was established by the method of thread embolization. After 2 h of ischemia, the thrombus was re-injected. The rats in each intervention group were treated with the same dose of Rb1ip qd × 7 d for 3 h after the last administration Middle cerebral artery occlusion model and reperfusion; sham operation group did not insert thread plug, the same operation. Twenty-four hours after operation, TTC staining was used to measure the infarct volume, the wet and dry weight of brain tissue were measured. The number of apoptotic cells and the expression of NgR were detected by immunohistochemistry. Results The infarct volume in each intervention group was (27.629 ± 1.401)% at 30 mg / kg, 24.164 ± 1.710% at 60 mg / kg and 21.955 ± 2.556% at 90 mg / kg, respectively 29.846 ± 1.153)% respectively. The brain water content of the rats in the sham operation group was 30 mg / kg (80.079 ± 0.726)%, 60 mg / kg (78.984 ± 0.902)% and 90 mg / kg (76.517 ± 0.37)% and (81.799 ± 1.065)%, respectively. The number of apoptotic cells was 30 mg / kg (89.000 ± 10.296), 60 mg / kg (59.000 ± 12.522) and 90 (36.667 ± 19.054) mg / kg and (1.600 ± 1.517) and (132.667 ± 22.223), respectively; the positive area of NgR expression was 30 mg / kg (84.827 ± 3.870) mg / kg group (66.040 ± 5.541) and 60 mg / kg group (75.577 ± 7.150), respectively, and those in sham group and ischemia group were (48.355 ± 9.720) and (91.485 ± 5.822), respectively. Conclusion Ginsenoside Rb1 has a protective effect on experimental cerebral ischemia in rats, which can reduce cerebral edema, infarct size and cell apoptosis induced by ischemia-reperfusion injury in a dose-dependent manner. The intervention of NgR expression suggests that Rb1 may play a role in the neuroplasticity after cerebral ischemia.