目的 :观察养阴通脑颗粒对大鼠脑缺血后脑组织内皮素 1( ET 1)基因表达的干预作用 ,探讨其对脑缺血损伤保护作用的机制。方法 :应用原位杂交及图像分析技术观察脑缺血侧皮质 ET 1基因表达的变化。结果 :缺血组与养阴通脑颗粒组缺血侧皮...目的 :观察养阴通脑颗粒对大鼠脑缺血后脑组织内皮素 1( ET 1)基因表达的干预作用 ,探讨其对脑缺血损伤保护作用的机制。方法 :应用原位杂交及图像分析技术观察脑缺血侧皮质 ET 1基因表达的变化。结果 :缺血组与养阴通脑颗粒组缺血侧皮质 ET 1基因表达显著高于自身健侧相应脑区 ,养阴通脑颗粒组缺血侧皮质 ET 1基因表达显著低于模型组缺血侧。结论 :脑缺血后脑组织 ET 1基因表达增高 ,养阴通脑颗粒可显著抑制缺血侧皮质 ET 1基因表达 ,对脑缺血性损伤具有保护作用。展开更多
Objective. The experiment was designed to study the association of cerebral ischemia and reperfusion with endothelin- 1 (ET- 1) gene expression of rat brains and time-dependent changes of ET- 1 gene expression during...Objective. The experiment was designed to study the association of cerebral ischemia and reperfusion with endothelin- 1 (ET- 1) gene expression of rat brains and time-dependent changes of ET- 1 gene expression during cerebral ischemia.Materials and methods. Thirty- three male SD rats were divided into dot blot hybridization(n = 27) and in silu hybridization groups(n= 6). The focal cerebral ischemia and reperfusion models were made with suture embolism of middle cerebral artery. Dot blot hybridization groups were redivided into control and ischemic subgroups (ischemia for 0. 5 , 1 , 1. 5 , 3 , 6 , 12 , 24 , 48 and 72 h respectively). In situ hybridization groups were redivided into ischemia and reperfusion groups. After 24 h ischemia and 24 h reperfusion,ET1 gene expressions were investigated with in situ hybridization and the resuhs were analyzed with IBAS 2000 Image Analysis System.Results. Dot blot hybridization showed that ET-1 mRNA of cerebral cortex and caudate- putamen was increased at 6 h of ischemia and reached peak at 24 h (3. 9 and 3. 7 fold respectively) ,and at 72 h of ischemia it remained at high levels(3. 5 and 2. 1 fold respectively). In silu hybridization showed that the levels of ET- 1 mRNA of cerebral cortex and caudate-putamen were also markedly increased both in 24 h ischemia and 24 h reperfusion groups (P<0. 01 , P<0. 05 respectively) .Conclusions. ET-1 gene expression in focal ischemic brain tissue were markedly and progressively increased during cerebral ischemia and reperfusion and downregulation of ET- 1 gene expression may be a new approach to the treatment of ischemic cerebrovascular diseases.展开更多
文摘目的 :观察养阴通脑颗粒对大鼠脑缺血后脑组织内皮素 1( ET 1)基因表达的干预作用 ,探讨其对脑缺血损伤保护作用的机制。方法 :应用原位杂交及图像分析技术观察脑缺血侧皮质 ET 1基因表达的变化。结果 :缺血组与养阴通脑颗粒组缺血侧皮质 ET 1基因表达显著高于自身健侧相应脑区 ,养阴通脑颗粒组缺血侧皮质 ET 1基因表达显著低于模型组缺血侧。结论 :脑缺血后脑组织 ET 1基因表达增高 ,养阴通脑颗粒可显著抑制缺血侧皮质 ET 1基因表达 ,对脑缺血性损伤具有保护作用。
文摘Objective. The experiment was designed to study the association of cerebral ischemia and reperfusion with endothelin- 1 (ET- 1) gene expression of rat brains and time-dependent changes of ET- 1 gene expression during cerebral ischemia.Materials and methods. Thirty- three male SD rats were divided into dot blot hybridization(n = 27) and in silu hybridization groups(n= 6). The focal cerebral ischemia and reperfusion models were made with suture embolism of middle cerebral artery. Dot blot hybridization groups were redivided into control and ischemic subgroups (ischemia for 0. 5 , 1 , 1. 5 , 3 , 6 , 12 , 24 , 48 and 72 h respectively). In situ hybridization groups were redivided into ischemia and reperfusion groups. After 24 h ischemia and 24 h reperfusion,ET1 gene expressions were investigated with in situ hybridization and the resuhs were analyzed with IBAS 2000 Image Analysis System.Results. Dot blot hybridization showed that ET-1 mRNA of cerebral cortex and caudate- putamen was increased at 6 h of ischemia and reached peak at 24 h (3. 9 and 3. 7 fold respectively) ,and at 72 h of ischemia it remained at high levels(3. 5 and 2. 1 fold respectively). In silu hybridization showed that the levels of ET- 1 mRNA of cerebral cortex and caudate-putamen were also markedly increased both in 24 h ischemia and 24 h reperfusion groups (P<0. 01 , P<0. 05 respectively) .Conclusions. ET-1 gene expression in focal ischemic brain tissue were markedly and progressively increased during cerebral ischemia and reperfusion and downregulation of ET- 1 gene expression may be a new approach to the treatment of ischemic cerebrovascular diseases.
