| Research on the mechanism and treatment of ischemic cerebral injury hasbeen always emphasized. In focal cerebral infarction neuron regeneration,structure reformation and plasticity have been recently emphasized highly.MAP-2 ,GAP-43 play important roles in neuron development, axonregeneration, synapsis growth and structure reformation. MAP-2,GAP-43 arethe important substance base of neural plasticity. Right now one of the mostcurrent problems is to choose the effective methods (including rehibilitationand drugs, etc.) to hasten neural plasticity and renew brain function.The treatment of acute ischemic cerebrovascular diseases is mainlyconcentrated on renewing provision of oxygen and blood flow. Such drugs asthrombolytic, anticoagulant, antithrombocytic, free radical scavenger andneural protectant are administerd. Edaravone is a new type of free radicalscavenger. In acute cerebral infarction edaravone can reduce volume ofinfarction and protect neuron, which is reported in related experimentalresearch. But whether edaravone protects neuron by affecting plasticity isunknown.In this experiment models of MCAO of create rats are made. We observethe dynamic changes of MAP-2,GAP-43 at different time points of cerebralischemia and the effects how edaravone affects their expression and neuralfunction so as to provide the deeper theoretical principle . We measure the expression of MAP-2,GAP-43 of rats models in focalcerebral ischemia by immunohistochemical and hybridization in situ technique,observe the grades of neural functions and pathomorphological changes,intervene with free radical scavenger and analyze the expression of MAP-2,GAP-43 by images .The results indicate that there is increased expression ofMAP-2,GAP-43 in the surroundings of focal cerebral ischemia. With timepassing by, the expression becomes higher. There is obvious expression ofMAP-2 in the 1st and 3 rd d. GAP-43 remains at a high level. There are highergrades and slighter pathological changes in edaravone group than those incontrol group. Edaravone affects the expression of MAP-2,GAP-43. There ishigher expression of MAP-2 in the 1 s t and 3 r d and of GAP-43 in 1-14 dafter ischemia .The results indicate that there is obvious time-extent changes ofthe expression of MAP-2,GAP-43 , the substance base of neural plasticity infocal cerebral ischemia. There is obvious high expression of MAP-2 in theearly ischemic period. The expression of GAP-43 remains high constantlyafter ischemia, which may be related with changes of neural plasticity in thesurroundings of focal cerebral ischemia. With edaravone administered, neuralfunctions are promoted and neural injuries are relieved. At the same timeedaravone affects the expression of MAP-2,GAP-43 and enhances theexpression at different extent. Edaravone may protect neuron in focal cerebralischemia by affecting neural plasticity. The mechanism may be related to theelevated expression of MAP-2,GAP-43. It has been studied that the expression of MAP-2,GAP-43 in thesurrounding of cerebral infarction plays important role in neuron development ,axon regeneration, snapsis growth, reformation of structure and function. Aftercerebral infarction the expression of MAP-2,GAP-43 manifests in thedynamic constant developing process. There are several methods to promoteneuron growth and tissue reformation by increasing the expression of MAP-2,GAP-43. The functions of neural protectant as potential drugs of treatment areto protect ischemic neuron, especially in the surroundings of ischemic regions.Administering all kinds of methods to hasten the neural plasticity does goodfor renewing neural functions. Edaravone, a new type of free radical scavenger, is administered to treatingacute ischemic cerebrovascular diseases. The effects of anti-free radicalscavenger are studied very much, but whether it can affect the expression ofMAP-2,GAP-43 is yet unknown. So in this research on discussing the base ofdynamic changes of MAP-2,GAP-43 after 1-14 d of ischemia we observe the... |
