| As a part of central nervous system,the spinal cord is not only a junior centrum controling the motor or feel of limbs and the motor of viscera,but also a key structure communicating the brain with peripheral nervous system, where there are dense fasciculuses. So even there is a focal injury to the spinal cord, it can induce a severe result. The contact between the brain and the body below the injury plane is broken off, it can lead to hemiplegia or quadriplegia forever or accompanying with pain enhaced reflex of parasympatetic and motor. These years, the incidence of spinal cord injury rise with the development of architecture and communications. It is still a universal challenge to protect and restore the function of the injuried spinal cord. The spinal cord injury has two types, one is called the primary injury, the other is called the secondary injury. The primary injury happens in the moment of injury, which is caused by patches of bone penerating into the spinal cord or by the hernia of intervertebral discs resulted by shift or dislocation of bone fracture, it can not be cured. The secondary injury of the spinal cord is caused by various elements after primary injury, it is more severe than primary injury sometimes. In order to improve the outcome after a spinal cord injury, different therapeutic trials focus on the possibility to reduce the secondary injury and to preserve as many cells as possible in the perifocal regions.Nerve 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 HSP27, can protect nerve cells by avariety of mechanisms. In central nervous system,a prior sublethal stimuli, such as heat shock or focal ischemia, will lead to induction of HSP27 and protection against a 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 has already helped organes overexpress HSP27 in destinative tissues and cells, including central nerve system and nerve cells, but it is successful only on the culture cells and some animals. Although gene technique will have a good prospect,it is still a long way for us to go.At present,there is a important significance for prevention and treatment of spinal cord injury, if we can induce the overexpression of HSP27 in a safe and efficient way 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 s pinal cord injury. There is an active significance to induce overexpression of HSP27 by using drug in operation in these cases, which can help protecting spinal cord and nerve function. Methylprednisolone has been the only one drug that the FDA(Food and Drug Administration) of America give an approval to be used to treat acute spinal cord injury. The standard program of MP(Methylprednisolone) to treat SCI(Spinal Cord Injury) patients has been extensively used all over the world. Study indicate that MP protect spinal cord by avariety of mechanisms. But there is still not a correlative report that whether MP can protect spinal cord at some extent by inducing the expression of HSP27.This study is to discover whether MP protect spinal cord at some extent by inducing the expression of HSP27 through such methods such as making animal models of acute spinal cord injury, using a large dose of Methylprednisolone within 8 hours after SCI(Spinal Cord Injury),detecting the expression of the HSP27 of rats'spinal cord by immunohistochemstry in operation,SCI,SCI with a large dose of Methylprednisolone in an early period(within 8 hours).Methods50 female SD rats,average 240g, were randomly divided into three groups: operation group(10 rats); acute spinal cord injury groups(20 rats); acute spinal cord injury group with MP treatment(20 rats).Allen's weight drop model was used for the second and the third group. The first and the second group's rats were poured into 0.9 % salt water with the same dose of the third group though tail vein within 5min after operation or SCI. The third group's rats were poured into Methylprednisolone in an early period(within 5min) by the doze of 30mg/kg. 24 hours later, the spinal cords were taken out and cut ,then the pathological changes of spinal cord cells with HE staining and the expression of HSP27 in spinal cord cells with immunohistochemical staining were observed respectively. The data were analysed with SPSS12.0 soft ware.Results1.There were significantly haemorrhage, edema, degeneration,vacuole and so on in spinal cord after SCI in rats.2.The expression of HSP27 show weak positive in the OP group and obviouly increase in the SCI group.3.The secondary injury of spinal cord is significantly improved in MP group. The expression of HSP27 significantly increased and show strong positive. 4.In the expression of HSP27,there is a significant difference between OP group and SCI group (P<0.01); there is also a significant difference between SCI group and MP group.Conclusions1.Avariety of stimuli can induce nerve cells of the spinal cord to express HSP27. 2.The expressive level of HSP27 vary from stimulus in tensity to stimulus type. Large-dose MP can obviously increase the expression of HSP27, improve the pathologic change and nerve function of the spinal cord. 3. MP can protect spinal cord by inducing nerve cells overexpressing HSP27 after spinal cord injury. |
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