The Effects Of The Expression Of ERK1/2on Autophagy In Cerebral Ischemia/reperfusion Injury In Rats

Objective：To investigate the correlation of extracellular regulated protein kinase1andextracellular regulated protein kinase2(ERK1/2) and autophagy by observing and recordingthe expression degree of ERK1/2protein and autophagy-related proteins：beclin1andmicro-tubule-associated protein1light chain3II (LC3-II)．Method：1The same batch healthy Wistar rats were divided into five groups randomly：shamgroup，model group and administration group， model group and administration group weredivided into two groups respectively：ischemia1hour reperfusion24hours group andischemia3hours reperfusion24hours group．2The rats were given ischemia for1hour or3hours by using suture method toestablish the middle cerebral artery occlusion model (MCAO)，and use extracellularregulated protein kinase kinase (MEK1/2) inhibitor-U0126to interference MCAO toestablish the administration group．3When established the MCAO，then，conduct the neuroethology assessment at24hours after reperfusion，which the higher the score was，the more severe the neurologicimpairment was．4The rats were sacrificed by given high dose of anesthetics when conducted theneuroethology assessment．5To calculate the cerebral infarct volume of rats in ischemic/reperfusion model(I/R)in five groups by2，3，5-triphenyltetrazolium chloride (TTC) staining method and do thestatistics analysis．6Observing the change of cytomorphology by hematoxylin-eosin staining (HE)staining method．7Observing and recording the expression degree of ERK1/2，beclin1and LC3-II bywestern blot，and do the statistics analysis． Results：1In the ischemia/reperfusion jnjury in rats，with increasing of ischemia time，theexpression of ERK1increased，and the expression of phospho-ERK1/2，beclin1，LC3-IIreduced， being associated with worse capacity， bigger infarct valume and moremorphological variation and death of cellular．2Autophagy was activited to protect the cerebral cells when get slight cerebralischemia injury，and inhibited as the injury aggrevated，then，damage of cerebral cells wasdeteriorated，either．3The expression of Autophagy-related proteins：LC3-II in administration group ismore than that of model group when had been used U0126with the dose of0．4576mg/kg tointerference the model of ischemia3hours and reperfusion24hours injury．...