| BackgroundThe cerebral infarction is a common disease which endangers the old people, and also is one of the most important reasons that causing death and mutilation, for recent years it is from the level of system and molecular to study the pathophysiological of ischemic cerebrovascular disease, which have made a great progress. The auto-compensation of angiogenesis after cerebral ischemia offers new ideas for studying the mechanism of ischemic cerebrovascular disease. The results that get from the young animals are very different from clinical practice. The morbidity and mortality of the gerontal patient suffering cerebral infarction is closely related to their affectivity and serious injure. TCM which treats ischemic stroke has significant effect, but the angiogenesis that traditional Chinese medicine promote the cerebral ischemical reperfusion injury have few reported. This study is based on the previous research to explore the mechanism of angiogenesis after ischemia reperfusion and the mechanism of action of Naomaitong promote angiogenesis from the levels of cell, molecule and gene. Objective1. To reveal the mechanism of cerebral ischemia reperfusion angio- genesis of gerontal patient from cerebral ischemia reperfusion angiogenesis of the aging rats.2. To investigate the pathophysiological character of cerebral ischemia reperfusion injury of gerontal patient basing on auto-compensation angiogenesis of aging rats.3. To investigate the mechanism of action of Naomaitong promoting cerebral ischemia reperfusion angiogenesis of aging rats.4. To evaluate the effect of Naomaitong on ischemia reperfusion injury of gerontal patient from promoting angiogenesis.Method1. The differences of the brain tissue moisture capacity, infarct size, apoptosis, ultrastructural orgnization, microvessel count of brain tissue, expressions of VEGF, TGF- β 1, bFGF and mRNA expressions of VEGF, VEGFR, TGF-β 1 are compared between aging rats and young rats at ischemia 3h andreperfusion Id,3d, 6d, 12d by light microscope, electron microscrope,immunohistocheraistry, hybridization in situ etc. 2. In light of the theory of TCM, we studied the mechanism of action of Naomaitongpromoting the angiogenesis after cerebral ischemia reperfusion of aging ratsfrom the expressions of VEGF, TGF, bFGF and the changes of mRNA expressionsof VEGF, VEGFR, TGF-Plo Result1. The cerebral angiogenesis of aging rats after ischemia reperfusion and the effect of Naomaitong promoting the cerebral angiogenesis .(1) The nerve function score: The score of aging model I 3h and I/R 6d was higher than that of young model in the same time (P<0. 05, P<0. 01), and the score of aging rats I/R Id was the highest. The nerve function score at I/R6d, 12d was low in the Naomaitong comparing the nimodipine (P<0.05). (2) The brain tissue moisture capacity: Aging rats appeared obviously hydrops after cerebral ischemia 3h, and the peak at Id. The cerebral edema begin obviously alleviating after 6d; the brain tissue moisture capacity at I/R Id, 3d, 6d of the Naomaitong group was lower than that of aging model (P<0. 01, P<0. 05). (3) The infarct size: The size at I3h, I/R3d of aging model was larger than that of young model (P<0. 05, P<0. 01). The size of aging rats get the peak at 3d and lasting to 6d; the peak of aging rats was higher than that of young rats. The size of Naomaitong was lower than that of aging model and the nimodipine in the same time point (P<0. 05, P<0. 01). (4) The apoptosis: The apoptosis count of aging sham operation and aging model was increased at I/R3d, 6d comparing with young model in the same times (P<0. 01). The apoptosis count of aging rats was arrived the peak in 3d. In addition, the count of the nimodipine and the Naomaitong group was reduced comparing with aging model at I/Rld, 3d, 6d, 12d(P<0. 01). The apoptosis count at I/R3d, 6d of Naomaitong group was fewer than that of nimodipine group (P<0. 01). (5)The ultrastructural orgnization of brain cell: The changes of neurons, gliocytes, vascular endothelial cell of model which treated by Naomaiton...
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