| Stroke is the number one cause of national death.In many cases,severe stroke symptoms can lead to disability.Although most strokes occur in people over 65,they can occur in young people.The average age of stroke in China is 66 years old,10 years earlier than that of white americans,and one fifth of the patients are less than 45 years old.The causes of cerebral apoplexy are complex,including vascular wall lesions,hemorheological and blood component abnormalities,heart disease and hemodynamic abnormalities,and others.The specific pathogenesis of the disease has not been clarified,and is often involved in oxidative stress,tissue edema,activation of inflammatory mediators and other related reactions.After acute cerebral artery occlusion,a series of pathophysiological changes occur in brain tissue.Continuous interruption of cerebral blood flow for 5min will lead to irreversible damage or even death of nerve cells."Ischemic penumbra" is an ischemic region located around the focal area of ischemic necrosis.Cerebral blood flow is between electrical failure(15～18ml?100g-1?min-1)and energy depletion(10～12ml?100g-1?min-1).The existence time of "ischemic penumbra" is related to various factors,and collateral circulation plays a decisive role.The existence of ischemic penumbra provides a histological basis for the decision of vascular recanalization in acute ischemic stroke.Previous experimental studies have shown that cerebral ischemic preconditioning can activate the endogenous protection mechanism of brain tissue.By studying the changes of brain tissue related factors after cerebral ischemic preconditioning,the protection mechanism of cerebral ischemic preconditioning on brain tissue can be further clarified.However,at present,there are few studies using the cerebral ischemicl prconditioning model to explore whether cerebral ischemicl preconditioning promotes neuroprotective effects through the Kir6.1/K-atp channel.To further explore the mechanism of ischemicl preconditioning on brain protection,in this study,experimental rat model of cerebral ischemic preconditioning was used to investigate the mechanism of Kir6.1/K-atp channel in ischemic brain injury,so as to provide a new theoretical basis for the treatment of pathological injury induced by cerebral ischemia.SPF male SD rats were provided by hua fukang animal experimental center and weighed 220-20 g.All experimental rats are kept in a constant temperature and humidity environment,and can eat and drink freely.Seventy-two patients were randomly divided into three groups(n=24):sham operation group,cerebral ischemia model group and cerebral ischemia preconditioning group.In the establishment of cerebral ischemia model,the right middle cerebral artery of rats was emblolized by the method of Zea Longa for 2 hours.in the ischemic preconditioning group,middle cerebral artery embolization was given for 10 minutes in advance,and then the tegline was gently extracted from the external carotid artery to complete the preischemia.Three days later,the rats were anesthetized again,and the rats were given middle cerebral artery embolization for 2hours.The procedure was the same as the model group.in the sham group,only the right common carotid artery was isolated.After rats awake after surgery Zea-Longa score,and 12 hours,24 hours,after surgery,36 hours,48 hours,each group of the experimental rats was evaluated by TTC method infarction area percentage,Western blot test on apoptosis and mitochondrial membrane protein Kir6.1/K-atp channel m TPT expression,transformation of hole detection kit and mitochondrial membrane potential kit(JC-1)detection of mitochondrial membrane potential and mitochondrial membrane permeability change.this study found that ischemic preconditioning can significantly improve the experimental rats Zeal Longa score results;And the thrombus volume was significantly different from the model group after 24 hours(p<0.05);The results of apoptotic proteins showed that compared with the sham group,the expression levels of apoptotic proteins Bax,Caspase-3 and Cyt-c in the brain tissues of rats in the model group increased significantly after 48 hours of modeling(p<0.05),while the expression levels of bcl-2 did not change significantly(p>0.05),indicating that cerebral ischemia accelerated and promoted the expression of apoptotic proteins.In addition,ischemic preconditioning can also improve the regulation of the expression of Kir6.1/K-atp channel in the mitochondrial membrane of experimental rats caused by brain injury,inhibit the increase of mitochondrial membrane.Therefore,ischemic preconditioning can effectively block or weaken the neurological damage and neuronal apoptosis caused by cerebral ischemia,inhibit neuronal apoptosis and regulate the expression of Kir 6.1,and reduce the permeability of mitochondrial transmembrane potential and mitochondrial membrane potential,which may be closely related to the regulation of Kir6.1/K-atp pathway. |
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