| BackgroundCerebral apoplexy has become the first disabling and lethal disease in China,among which ischemic cerebrovascular disease has seriously affected people’s health and life.As soon as possible to restore brain blood and oxygen supply for special meaning to reduce disability fatality rate,however,after the blood and oxygen supply for recovery may appear more serious damage,namely the cerebral ischemia-reperfusion injury,it mainly includes the calcium overload,inflammation,such as damage mechanism,widely attention of inflammatory reaction mechanism,as a transcription factor regulating inflammation and cause of target gene expression to increase the nf-kappa B become the research hot spot.Drug preconditioning of cerebral ischemia refers to the preconditioning of brain reperfusion injury with drugs to induce the body to form neural protection in order to avoid or alleviate irreversible injury.Adenosine is an important endogenous active substance in the body,and its signal transduction is realized by regulating inflammatory response,ischemic tissue injury and tissue remodeling.A large number of experiments have proved that adenosine preconditioning can effectively alleviate the neurological impairment caused by cerebral blood-reperfusion injury in rats,and it is of great significance to improve the molecular mechanism of its protective effect on the brain for the early safe and effective application of adenosine in clinical prevention of cerebral ischemia-reperfusion injury.ObjectiveBy observing the effects of adenosine preconditioning on TNF-αand NF-κB after cerebral ischemia reperfusion injury in rats,the molecular protective mechanism of adenosine on cerebral ischemia reperfusion injury in rats was investigated.MethodsSixty Sprague-Dawley rats were randomly divided into sham operation group(F group),ischemia-reperfusion group(IR group)and adenosine preconditioning ischemia-reperfusion group(AP group),and each group was randomly divided into 5 rats at the four time points of 2h,6h,24h and 48h after ischemia-reperfusion.The model of middle cerebral artery occlusion in rats was established by MCAO method.Based on the above three groups of 48 h after cerebral ischemia-reperfusion rats line organization head MRI,HE staining,and for more than 60 neural function defect scale in rats,integral optical density of the software system by immunohistochemical method in the observation group rats TNF alpha and nf-kappa B average integral optical density value to further verify the adenosine preconditioning on rat cerebral ischemia-reperfusion injury,adenosine on rat ischemia-reperfusion injury of protection mechanism.Results1.The rats in group F showed no signs of neurological impairment after surgery,while the rats in group AP and IR showed obvious signs of neurological impairment after surgery.The scores of neurological deficits in AP group and IR group were significantly higher than those in F group,and those in AP group were significantly lower than those in IR group,with statistically significant differences(P<0.05).2.There were no significant abnormalities in T1WI and T2WI in postoperative MRI of the rats in group F,the volume of cerebral infarction in the rats in group AP and IR was significantly higher than that in group F,and the volume of cerebral infarction in the rats in group AP was significantly lower than that in group IR,The volume of cerebral infarction measured in IR group was(168.80±17.584)mm~3,and that in AP group was(66.80±7.694)mm~3,with statistically significant differences(P<0.05).3.Under the light microscope,the nerve cells in the hippocampus of the rats in group F were orderly arranged,with complete neuron structure,weak nuclear staining,abundant nissite,and no edema in the neural matrix.Neurons in IR group showed necrotic changes,with fuzzy structure,cell body swelling,unclear boundary between nucleus and cytoplasm,and wide and transparent areas around them.Brain tissue around the infarct is swollen,glial cells increase,and some nerve cells shrink and lyse.The HE staining of AP group was similar to that of IR group,but lighter than that of IR group,with relatively complete cell structure and tissue hierarchy.4.The expressions of TNF-αand NF-κB in AP group and IR group were significantly higher than those in F group,while the expressions of TNF-αand NF-κB in AP group were significantly lower than those in IR group,Statistical results P<0.05,indicating that the difference was statistically significant.Conclusionadenosine preconditioning can reduce the expression of TNF-αand NF-κB in the brain of rats after ischemia-reperfusion injury,so as to reduce the damage of nerve cells. |
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