Autophagy has been suggested to participate in the pathology of hypoxic-ischemic brain damage（HIBD）.However,its regulatory role in HIBD remains unclear and was thus examined here using a rat model.To induce HIBD,the...Autophagy has been suggested to participate in the pathology of hypoxic-ischemic brain damage（HIBD）.However,its regulatory role in HIBD remains unclear and was thus examined here using a rat model.To induce HIBD,the left common carotid artery was ligated in neonatal rats,and the rats were subjected to hypoxia for 2 hours.Some of these rats were intraperitoneally pretreated with the autophagy inhibitor 3-methyladenine（10 m M in 10 μL） or the autophagy stimulator rapamycin（1 g/kg） 1 hour before artery ligation.Our findings demonstrated that hypoxia-ischemia-induced hippocampal injury in neonatal rats was accompanied by increased expression levels of the autophagy-related proteins light chain 3 and Beclin-1 as well as of the AMPA receptor subunit GluR 1,but by reduced expression of GluR 2.Pretreatment with the autophagy inhibitor 3-methyladenine blocked hypoxia-ischemia-induced hippocampal injury,whereas pretreatment with the autophagy stimulator rapamycin significantly augmented hippocampal injury.Additionally,3-methyladenine pretreatment blocked the hypoxia-ischemia-induced upregulation of Glu R1 and downregulation of GluR2 in the hippocampus.By contrast,rapamycin further elevated hippocampal Glu R1 levels and exacerbated decreased GluR2 expression levels in neonates with HIBD.Our results indicate that autophagy inhibition favors the prevention of HIBD in neonatal rats,at least in part,through normalizing Glu R1 and GluR2 expression.展开更多
Objective:To describe the clinical features of autoimmune encephalitis complicated with gastrointestinal hemorrhage.Methods:The clinical data of one patient whose initial symptom was mental abnormality were collected ...Objective:To describe the clinical features of autoimmune encephalitis complicated with gastrointestinal hemorrhage.Methods:The clinical data of one patient whose initial symptom was mental abnormality were collected and the related examinations,such as cerebrospinal fluid and magnetic resonance imaging (MRI),were improved.Results: Cerebrospinal fluid examination found that anti-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor(AMPAR)2 antibody was strongly positive,although the patient had repeated gastrointestinal hemorrhage but,after hormone combined with immunoglobulin treatment,the symptoms gradual-ly improved.Conclusion:Mental disorders are not all psychosis,and autoimmune encephalitis should not be ignored.It is very important to perform anti-AMPAR encephalitis antibody test;accurate diagnosis and timely treatment can improve the prognosis.展开更多
基金supported by the National Natural Science Foundation of China,No.81471488,81271378,81502157,and 81501291the Key Medical Subjects of Jiangsu Province of China,No.XK201120+3 种基金the Jiangsu Province Key Research and Development of Special Funds in China,No.BE2015644the Science and Technology Project of Suzhou City of China,No.SYSD2013105,SYS201446,SYS201441the Public Health Technology Project of Suzhou City of China,No.SS201536the Department of Pediatrics Clinical Center of Suzhou City of China,No.Szzx201504
文摘Autophagy has been suggested to participate in the pathology of hypoxic-ischemic brain damage（HIBD）.However,its regulatory role in HIBD remains unclear and was thus examined here using a rat model.To induce HIBD,the left common carotid artery was ligated in neonatal rats,and the rats were subjected to hypoxia for 2 hours.Some of these rats were intraperitoneally pretreated with the autophagy inhibitor 3-methyladenine（10 m M in 10 μL） or the autophagy stimulator rapamycin（1 g/kg） 1 hour before artery ligation.Our findings demonstrated that hypoxia-ischemia-induced hippocampal injury in neonatal rats was accompanied by increased expression levels of the autophagy-related proteins light chain 3 and Beclin-1 as well as of the AMPA receptor subunit GluR 1,but by reduced expression of GluR 2.Pretreatment with the autophagy inhibitor 3-methyladenine blocked hypoxia-ischemia-induced hippocampal injury,whereas pretreatment with the autophagy stimulator rapamycin significantly augmented hippocampal injury.Additionally,3-methyladenine pretreatment blocked the hypoxia-ischemia-induced upregulation of Glu R1 and downregulation of GluR2 in the hippocampus.By contrast,rapamycin further elevated hippocampal Glu R1 levels and exacerbated decreased GluR2 expression levels in neonates with HIBD.Our results indicate that autophagy inhibition favors the prevention of HIBD in neonatal rats,at least in part,through normalizing Glu R1 and GluR2 expression.
基金Undergraduate Innovation and Entrepreneur-ship Program Project of Hubei University of Medicine(X202210929021)Scientific research program of Hubei Provincial Department of education in 2019(Q20192103).
文摘Objective:To describe the clinical features of autoimmune encephalitis complicated with gastrointestinal hemorrhage.Methods:The clinical data of one patient whose initial symptom was mental abnormality were collected and the related examinations,such as cerebrospinal fluid and magnetic resonance imaging (MRI),were improved.Results: Cerebrospinal fluid examination found that anti-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor(AMPAR)2 antibody was strongly positive,although the patient had repeated gastrointestinal hemorrhage but,after hormone combined with immunoglobulin treatment,the symptoms gradual-ly improved.Conclusion:Mental disorders are not all psychosis,and autoimmune encephalitis should not be ignored.It is very important to perform anti-AMPAR encephalitis antibody test;accurate diagnosis and timely treatment can improve the prognosis.
