| Ischemia reperfusion injury (IRI) is the phenomenon in which the injury of the tissues and the organs getting more and more serious after being reperfused on the basic of ischemia. At present, the mechanism of IRI is still in the argument. But what is known in common about IRI is that IRI is a prosess from a reversible injury—ischemia injury to an unreversible injury—reperfusion injury. In the now days, cardiovascular diseases are contracting more and more frequently, and myocardium is in the danger of IRI.About the mechanism of IRI there are mainly falling several theorys: 1,calcium overload. 2,the activation of the apoptosis gene. 3,no-reflow. 4,effects of excitatoty amino acids. 5,the disorder of mitochondria function. And to serve as a go-between those theorys is the importance of free radicals in the prosess of IRI. So in our experiment, we designed and made a model in which the myocardiums of rats were injured by ischemia reperfusion. Then we used lipoic acid (LA) as a factor of intervation to observe the different degree of myocardium injury. In this way, we tried to find the target by which the free radicals did harm to the myocardium in the prosess of ischemia-reperfusion, and to find the possible mechanisms of the injury. On which we want to get some useful ways to prevention and cure the myocardium IRI. The extensional results of our experiments are as follow:1 The ischemia-reperfusion-injury model of myocardiums in rats was successfully improved, and electrocardiogram was chosed to ensure that prosseses of ischemia reperfusion had really happened.2 The signal enzyme of myocardial injury both in tissue homogenate and in blood serum were stepping up, the activities of antioxidase were stepping down, and the contents of the outputs from oxidation were becoming more and more.All of those told us a fact: the IR had induced the myocardium into the oxidative injury, and made both the myocardium and the whole body be in the state of oxidative stress. After we gived the LA to the rats, we observed that the activities of antioxidase were going to rise, the contents of the outputs from oxidation were growing downwards.So from those results, we get this conclusion: LA can both keep up the activities of antioxidase and reduce the outputs of oxidation, from which it keeps the myocardium away from oxidative injury induced by IR.3 The resuls of RT-PCR about COX-2 mRNA and the Western-blot about NF-κB p65 disclosed LA could cut down the expression of COX-2 mRNA and the contents of NF-κB p65 in the IRI myocardial nuclei (P<0.05).And the results of IR myocardial sections by immunohistochemical staining disclosed LA could also depress the presence of ICAM-1 on the surface of vascular endothelial cell. So from those results, we get this conclusion: LA could depress the expression of some factors which could induce inflammation, and then the degree of infection of the IR myocardium is descented, the injured myocardium induced by IR is protectd by LA.4 The results of DNA gel electrophoresis disclosed the injury of myocardial DNA was released in LA+IRx.It can be seen that LA could protect the myocardium against the injury induced by IR, from keeping the myocardium away from oxidative injury, pulling down the degree of infection of the IR myocardium and the whole body, and releasing the breaking down of myocardial structure.
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