Expression Of ATG1 And LC3B In Rat Brain After Ischemia Reperfusion Injury

ObjectiveTo investigate the activation rule of ATG1, LC3 B in cerebral cortex after focal cerebral ischemia reperfusion injury(CIR), thereby exploring its effect on autophagy in brain cells.MethodsSD rats were randomly divided into sham operation group(Sham group) and model group. Model group has been divided into cerebral ischemia reperfusion(IR) 0h、0.5h、1h、3h、6h 、12h、24h、72h nine subgroups. Rat CIR models were established using middle cerebral artery occlusion(MCAO). Neurological function score, TTC staining and the water content of brain tissue were used to evaluate the CIR model. Autophagy in brain cells were explored after CIR damage using electron microscopy. And immunohistochemistry and Western blot were used for qualitative and quantitative detection of ATG1 and LC3 B in cerebral cortex.ResultsCompared with the Sham group, IR 24 h group showed obvious symptoms of neurological impairment, brain water content increased, and clear cerebral infarction, which confirmed the successful preparation of MCAO model.CIR can occur brain cell autophagy. Immunohistochemical staining and Western blot showed that ATG1, LC3 B in the Sham group and the IR 0h group show faint bands. Obvious bands was observed in IR 0.5h. With the extension of ischemic time, the band of expression was enhanced and reached the peak in IR 1h, then gradually decreased. A second peak appears at IR12 h, then the expression is gradually decreased. By correlation analysis test results showed that in rat brain cortex and protein expression of LC3 B and ATG1 protein was positively correlated.ConclusionATG1 and LC3 B play key roles in the regulation of autophagy after CIR.