| It's still very difficult to protect and recover nerve function after spinal cord injury. A focal injury to the spinal cord may induce a cascade of pathophysiological events leading to cell and tissue necrosis. Neurons, glial cells and microvessels in segments of the cord around the primary injury will be exposed to a wide range of adverse alterations in their cellular and fluid microenvironment Some of the cells cannot withstand the changes and die:so-called secondary injuries. Other neurons and glial cells in the perifocal regions may resist the alterations in their environment and survive. In order to improve the outcome after a spinal cord injury, different therapeutic trials focus on the possibility to reduce the secondary injuries and to preserve as many cells as possible in the perifocal regionsNerve cells exposed to stressful stimuli will respond with a rapid production of so-called 'stress' or 'heat-shock' proteins (HSPs) . It is known from other experiments that some of HSPs ,such as HSP70, can protect nerve cells by a variety of mechanisms. In central nerve system,a prior sublethal stimuli ,such as heat shock or focal ischemia ,will lead to induction of HSP70 and protection against a subsequent severe insult .But so far,this way hasn't been able to be used in clinic,because we can't control the location,level and type of expression of HSPs and we also can't predict when the spinal cord injury will take place. Gene technique can have already helped organis overexpress HSP70 in destinative tissues and cells,including central nerve system and nerve cells ,but it get success only on the culture cells and a part of animal. Although gene technique will have a good prospect,we need waiting for a long time.At present, there is a important significance for prevention and treatment of spinal cord injury ,if we can induce the overexpression of HSP70 in a safe and efficient manner in spinal cord using pharmacological therapy procedures. Paralysis maybe will take place in some severe patients of spinal cord compression after operative discompression ,because of spinal cord ischemia and reperfusion injury. Corrective operation of deformities of the spine perhaps result to spinal cord injury. There is active significance to induce overexpression of HSP70 by using drug before operation in these cases, which can help protecting spinal cord and nerve function. Methylprednisolone has been only one a drug that the FDA of America give approval to be used to treat acute spinal cord injury. The standard program of MP to treat SCI has been extensively used all over the world. Study indicate that MP protect spinal cord by a variety of mechanism. But , there is not still correlative report that if MP can protectspinal cord at some extent by induce the expression of HSP70.This study is a part of foundational investigation on prevention and treatment of SCI. we detect the expression of the HSP70 in normal and traumatic spinal cord ,study the influence of MP on the expression of HSP70 and try to discover if MP protect spinal cord at some extent by inducing the expression of HSP70.Objective To study the expression of HSP70 in rat spinal cord around an injury to the spinal cord, and the influence of the high-dose methylprednisolone on the expression of the HSP70.Methods To create animal model of spinal cord injury applying the Allen's weight drop method. The first part: Sixty-five healthy adult Sprague-Dawley rats were randomly divided into three groups: Sample operation groups(OP groups, n=5); acute spinal cord injury groups ( SCI groups, n=5); Control groups(C groups ,n=5). To study the pathomorphology and HSP70 immunohistochemisty of spinal cord section at 2-hour, 6-hour, 12-hour, 24-hour, 48-hour and 72-hour after SCI, respectively. The second part: ninety healthy adult Sprague-Dawley rats were randomly divided into three groups: MP treatment groups(TR groups, n=5); MP Pretreatment groups ( PT groups, n=5); MP Control groups(CO groups ,n=5). To study the pathomorphology and HSP70 immunohistochemisty of spinal cord sectio...
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