Expression Of P75NTR And Changes Of Autophagy Function In Hemin Injured Neuron Model

Objective:Intracerebral hemorrhage(ICH)has high incidence,high mortality and poor prognosis.Neuronal apoptosis after Intracerebral hemorrhage is an important cause of residual disability and autophagy dysfunction may play a key role in the occurrence and progression of brain injury.P75 Neurotrophic Factor Receptor(P75 NTR)plays an important role in regulating neuronal apoptosis and autophagy.In this study,we investigated the changes of p75 NTR and autophagy related proteins after intracerebral hemorrhage using in vitro neuron injury model.To provide reference for neuron protection after intracerebral hemorrhage.Methods:In this study,hemin chloride(hemin)was used to damage mouse neuron HT22 cell lines to construct in vitro intracerebral hemorrhage related neuron injury model.The morphological changes of HT22 cells were observed by phase contrast microscope,and the optimal injury concentration of hemin was selected.Western Blot was used to detect the expression of apoptosis related proteins Bax,Bcl2,p75 NTR and autophagy related proteins P62(autophagy substrate SQSTM1)and LC3II.Results:In vitro experiments showed that the expression levels of apoptotisis related proteins Bax,Bcl2 and p75 NTR and autophagy related proteins P62 and LC3 II were significantly increased in HT22 cells treated with 100umol/L hemin for 6h compared with the control group.The difference was statistically significant,suggesting that hemin injury promoted neuronal apoptosis,and hemin injury could activate neuronal autophagosome formation,but there were autophagic flow disorders.Conclusion :After intracerebral hemorrhage,hemin damage may lead to increased expression of p75 NTR in neurons,autophagy dysfunction,and further aggravate neuronal apoptosis.