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Neuronal injury and tumor necrosis factor-alpha immunoreactivity in the rat hippocampus in the early period of asphyxia-induced cardiac arrest under normothermia

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Neural Regeneration Research 2017年第12期12卷 2007-2013页

作者： Hyun-Jin Tae Il Jun Kang Tae-Kyeong Lee jeong hwi cho Jae-Chul Lee Myoung Cheol Shin Yoon Sung Kim Jun hwi cho Jong-Dai Kim Ji Hyeon Ahn Joon Ha Park In-Shik Kim Hyang-Ah Lee Yang Hee Kim Moo-Ho Won Young Joo Lee Bio-Safety Research Institute College of Veterinary Medicine Chonbuk National University Iksan South Korea Department of Food Science and Nutrition Hallym University Chuncheon South Korea Department of Neurobiology School of Medicine Kangwon National University Chuncheon South Korea Department of Emergency Medicine School of Medicine Kangwon National University Chuncheon South Korea Department of Emergency Medicine Samcheok Medical Center Samcheok South Korea Division of Food Biotechnology School of Biotechnology Kangwon National University Chuncheon South Korea Department of Biomedical Science Research Institute of Bioscience and Biotechnology Hallym University Chuncheon South Korea Department of Obstetrics and Gynecology School of Medicine Kangwon National University Chuncheon South Korea Department of Surgery School of Medicine Kangwon National University Chuncheon South Korea Department of Emergency Medicine Seoul Hospital College of Medicine Sooncheonhyang University Seoul South Korea

Low survival rate occurs in patients who initially experience a spontaneous return of circulation after cardiac arrest（CA）. In this study, we induced asphyxial CA in adult male Sprague-Daley rats, maintained their body temperature at 37 ± 0.5°C, and then observed the survival rate during the post-resuscitation phase. We examined neuronal damage in the hippocampus using cresyl violet（CV） and Fluore-Jade B（F-J B） staining, and pro-inflammatory response using ionized calcium-binding adapter molecule 1（Iba-1）, glial fibrillary acidic protein（GFAP）, and tumor necrosis factor-alpha（TNF-α） immunohistochemistry in the hippocampus after asphyxial CA in rats under normothermia. Our results show that the survival rate decreased gradually post-CA（about 63% at 6 hours, 37% at 1 day, and 8% at 2 days post-CA）. Rats were sacrificed at these points in time post-CA, and no neuronal damage was found in the hippocampus until 1 day post-CA. However, some neurons in the stratum pyramidale of the CA region in the hippocampus were dead 2 days post-CA. Iba-1 immunoreactive microglia in the CA1 region did not change until 1 day postCA, and they were activated（enlarged cell bodies with short and thicken processes） in all layers 2 days postCA. Meanwhile, GFAP-immunoreactive astrocytes did not change significantly until 2 days post-CA. TNF-α immunoreactivity decreased significantly in neurons of the stratum pyramidale in the CA1 region 6 hours post-CA, decreased gradually until 1 day post-CA, and increased significantly again 2 days post-CA. These findings suggest that low survival rate of normothermic rats in the early period of asphyxia-induced CA is related to increased TNF-α immunoreactivity, but not to neuronal damage in the hippocampal CA1 region.

关键词： nerve regeneration post-cardiac arrest syndrome normothermia neuronal damage gliosis tumor necrosis factor-alpha neural regeneration

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Effect of hyperthermia on calbindin-D 28k immunoreactivity in the hippocampal formation following transient global cerebral ischemia in gerbils

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Neural Regeneration Research 2017年第9期12卷 1458-1464页

作者： Jae-Chul Lee jeong-hwi cho Tae-Kyeong Lee In Hye Kim Moo-Ho Won Geum-Sil cho Bich-Na Shin In Koo Hwang Joon Ha Park Ji Hyeon Ahn Il Jun Kang Young Joo Lee Yang Hee Kim Department of Neurobiology School of Medicine Kangwon National University Department of Pharmacology & Toxicology Shinpoong Pharmaceutical Co. Ltd. Department of Physiology College of Medicine Hallym University Department of Anatomy and Cell Biology College of Veterinary Medicine and Research Institute for Veterinary Science Seoul National University Department of Biomedical Science Research Institute of Bioscience and Biotechnology Hallym University Department of Food Science and Nutrition Hallym University Department of Emergency Medicine Seoul Hospital College of Medicine Sooncheonhyang University Department of Surgery School of Medicine Kangwon National University

Calbindin D-28K （CB）, a Ca2＋-binding protein, maintains Ca2＋ homeostasis and protects neurons against various insults. Hyperthermia can exacerbate brain damage produced by ischemic insults. However, little is reported about the role of CB in the brain under hyperthermic condition during ischemic insults. We inves- tigated the effects of transient global cerebral ischemia on CB immunoreactivity as well as neuronal damage in the hippocampal formation under hyperthermic condition using immunohistochemistry for neuronal nuclei （NeuN） and CB, and Fluoro-Jade B histofluorescence staining in gerbils. Hyperthermia （39.5 ＋ 0.2~C） was induced for 30 minutes before and during transient ischemia. Hyperthermic ischemia resulted in neu- ronal damage/death in the pyramidal layer of CA1-3 area and in the polymorphic layer of the dentate gyrus at 1, 2, 5 days after ischemia. In addition, hyperthermic ischemia significantly decreaced CB immunoreac- tivity in damaged or dying neurons at 1, 2, 5 days after ischemia. In brief, hyperthermic condition produced more extensive and severer neuronal damage/death, and reduced CB immunoreactivity in the hippocampus following transient global cerebral ischemia. Present findings indicate that the degree of reduced CB immu- noreactivity might be related with various neuronal damage/death overtime and corresponding areas after ischemic insults.

关键词： nerve regeneration hyperthermic condition ischemia/reperfusion injury subregions of hippocampus delayed neuronal death calbindin D-28k neural regeneration

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Activation of immediate-early response gene c-Fos protein in the rat paralimbic cortices after myocardial infarction

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Neural Regeneration Research 2015年第8期10卷 1251-1257页

作者： Ji Yun Ahn Hyun-Jin Tae jeong-hwi cho In Hye Kim Ji Hyeon Ahn Joon Ha Park Dong Won Kim Jun hwi cho Moo-Ho Won Seongkweon Hong Jae-Chul Lee jeong Yeol Seo Department of Emergency Medicine Sacred Heart Hospital College of Medicine Hallym University Department of Emergency Medicine School of Medicine Kangwon National University Department of Biomedical Science and Research Institute for Bioscience and Biotechnology Hallym University Department of Neurobiology School of Medicine Kangwon National University Department of Emergency Medicine Chuncheon Sacred Heart Hospital College of Medicine Hallym University Department of Surgery School of Medicine Kangwon National University

c-Fos is a good biological marker for detecting the pathogenesis of central nervous system disorders. Few studies are reported on the change in myocardial infarction-induced c-Fos expression in the paralimbic regions. Thus, in this study, we investigated the changes in c-Fos expression in the rat cingulate and piriform cortices after myocardial infarction. Neuronal degeneration in cingulate and piriform cortices after myocardial infarction was detected using cresyl violet staining, Neu N immunohistochemistry and Fluoro-Jade B histofluorescence staining. c-Fos-immunoreactive cells were observed in cingulate and piriform cortices at 3 days after myocardial infarction and peaked at 7 and 14 days after myocardial infarction. But they were hardly observed at 56 days after myocardial infarction. The chronological change of c-Fos expression determined by western blot analysis was basically the same as that of c-Fos immunoreactivity. These results indicate that myocardial infarction can cause the chronological change of immediate-early response gene c-Fos protein expression, which might be associated with the neural activity induced by myocardial infarction.

关键词： nerve regeneration paralimbic cortices myocardial infarction c-Fos cingulate cortex piriform cortex immunohistochemistry western analysis neural regeneration

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Neuroprotective effects of ischemic preconditioning on hippocampal CA1 pyramidal neurons through maintaining calbindin D28k immunoreactivity following subsequent transient cerebral ischemia

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Neural Regeneration Research 2017年第6期12卷 918-924页

作者： In Hye Kim Yong Hwan Jeon Tae-Kyeong Lee jeong hwi cho Jae-Chul Lee Joon Ha Park Ji Hyeon Ahn Bich-Na Shin Yang Hee Kim Seongkweon Hong Bing Chun Yan Moo-Ho Won Yun Lyul Lee Department of Neurobiology School of Medicine Kangwon National University Department of Radiology School of Medicine Kangwon National University Department of Biomedical Science Research Institute of Bioscience and Biotechnology Hallym University Department of Physiology College of Medicine Hallym University Department of Surgery School of Medicine Kangwon National University Institute of Integrative Traditional & Western Medicine Medical College Yangzhou University

Ischemic preconditioning elicited by a non-fatal brief occlusion of blood flow has been applied for an experimental therapeutic strategy against a subsequent fatal ischemic insult. In this study, we investigated the neuroprotective effects of ischemic preconditioning（2-minute transient cerebral ischemia） on calbindin D28k immunoreactivity in the gerbil hippocampal CA1 area following a subsequent fatal transient ischemic insult（5-minute transient cerebral ischemia）. A large number of pyramidal neurons in the hippocampal CA1 area died 4 days after 5-minute transient cerebral ischemia. Ischemic preconditioning reduced the death of pyramidal neurons in the hippocampal CA1 area. Calbindin D28k immunoreactivity was greatly attenuated at 2 days after 5-minute transient cerebral ischemia and it was hardly detected at 5 days post-ischemia. Ischemic preconditioning maintained calbindin D28 k immunoreactivity after transient cerebral ischemia. These findings suggest that ischemic preconditioning can attenuate transient cerebral ischemia-caused damage to the pyramidal neurons in the hippocampal CA1 area through maintaining calbindin D28k immunoreactivity.

关键词： hippocampal subsequent minute pyramidal maintaining attenuated hippocampus neuronal occlusion fatal

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Direct 4D printing of functionally graded hydrogel networks for biodegradable,untethered,and multimorphic soft robots

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International Journal of Extreme Manufacturing 2024年第2期6卷 407-416页

作者： Soo Young cho Dong Hae Ho Sae Byeok Jo jeong Ho cho Department of Chemical and Biomolecular Engineering Yonsei UniversitySeoul 03722Republic of Korea Department of Mechanical Engineering Virginia TechBlacksburgVA 24061United States of America School of Chemical Engineering Sungkyunkwan UniversitySuwon 16419Republic of Korea SKKU Institute of Energy Science and Technology(SIEST) Sungkyunkwan UniversitySuwon 16419Republic of Korea

Recent advances in functionally graded additive manufacturing(FGAM)technology have enabled the seamless hybridization of multiple functionalities in a single *** robotics can become one of the largest beneficiaries of these advances,through the design of a facile four-dimensional(4D)FGAM process that can grant an intelligent stimuli-responsive mechanical functionality to the printed ***,we present a simple binder jetting approach for the 4D printing of functionally graded porous multi-materials(FGMM)by introducing rationally designed graded multiphase feeder *** graded cross-linking agents gradually form stable porous network structures within aqueous polymer particles,enabling programmable hygroscopic deformation without complex mechanical ***,a systematic bed design incorporating additional functional agents enables a multi-stimuli-responsive and untethered soft robot with stark stimulus *** biodegradability of the proposed 4D-printed soft robot further ensures the sustainability of our approach,with immediate degradation rates of 96.6%within 72 *** proposed 4D printing concept for FGMMs can create new opportunities for intelligent and sustainable additive manufacturing in soft robotics.

关键词： intelligent and sustainable additive manufacturing multi-material four-dimensional printing untethered soft robot multi-stimuli-responsive soft robot biodegradable soft robotics

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Long-term administration of scopolamine interferes with nerve cell proliferation, differentiation and migration in adult mouse hippocampal dentate gyrus, but it does not induce cell death

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Neural Regeneration Research 2014年第19期9卷 1731-1739页

作者： Bing Chun Yan Joon Ha Park Bai Hui Chen jeong-hwi cho In Hye Kim Ji Hyeon Ahn Jae-Chul Lee In Koo Hwang Jun hwi cho Yun Lyul Lee Il-Jun Kang Moo-Ho Won Department of Integrative Traditional & Western Medicine Medical CollegeYangzhou University Department of Neurobiology School of MedicineKangwon National University Department of Physiology College of MedicineInstitute of Neurodegeneration and NeuroregenerationHallym University Department of Anatomy and Cell Biology College of Veterinary MedicineSeoul National University Department of Emergency Medicine School of MedicineKangwon National University Department of Food Science and Nutrition Hallym University

Long-term administration of scopolamine, a muscarinic receptor antagonist, can inhibit the survival of newly generated cells, but its effect on the proliferation, differentiation and migration of nerve cells in the adult mouse hippocampal dentate gyrus remain poorly understood. In this study, we used immunohistochemistry and western blot methods to weekly detect the biological behaviors of nerve cells in the hippocampal dentate gyrus of adult mice that received intraperito- neal administration of scopolamine for 4 weeks. Expression of neuronal nuclear antigen （NeuN; a neuronal marker） and Fluoro-]ade B （a marker for the localization of neuronal degeneration） was also detected. After scopolamine treatment, mouse hippocampal neurons did not die, and Ki-67 （a marker for proliferating cells）-immunoreactive cells were reduced in number and reac hed the lowest level at 4 weeks. Doublecortin （DCX; a marker for newly generated neurons）-im- munoreactive cells were gradually shortened in length and reduced in number with time. After scopolamine treatment for 4 weeks, nearly all of the 5-bromo-2＇-deoxyuridine （BrdU）-labeled newly generated cells were located in the subgranular zone of the dentate gyrus, but they did not migrate into the granule cell layer. Few mature BrdU/NeuN double-labeled cells were seen in the subgranular zone of the dentate gyrus. These findings suggest that long-term administration of scopolamine interferes with the proliferation, differentiation and migration of nerve cells in the adult mouse hippocampal dentate gyrus, but it does not induce cell death.

关键词： nerve regeneration neurogenesis scopolamine dentate gyrus cell proliferation neuroblastdifferentiation neuroblast migration granule cell layer neural regeneration

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Monocarboxylate transporter 4 plays a significant role in the neuroprotective mechanism of ischemic preconditioning in transient cerebral ischemia

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Neural Regeneration Research 2015年第10期10卷 1604-1611页

作者： Seongkweon Hong Ji Yun Ahn Geum-Sil cho In Hye Kim jeong hwi cho Ji Hyeon Ahn Joon Ha Park Moo-Ho Won Bai Hui Chen Bich-Na Shin Hyun-Jin Tae Seung Min Park Jun hwi cho Soo Young choi Jae-Chul Lee Department of Surgery School of Medicine Kangwon National University Department of Emergency Medicine Sacred Heart Hospital College of Medicine Hallym University Department of Emergency Medicine School of Medicine Kangwon National University Department of Neuroscience College of Medicine Korea University Department of Neurobiology School of Medicine Kangwon National University Department of Physiology College of Medicine Hallym University Department of Biomedical Science Research Institute of Bioscience and Biotechnology Hallym University

Monocarboxylate transporters（MCTs）, which carry monocarboxylates such as lactate across biological membranes, have been associated with cerebral ischemia/reperfusion process. In this study, we studied the effect of ischemic preconditioning（IPC） on MCT4 immunoreactivity after 5 minutes of transient cerebral ischemia in the gerbil. Animals were randomly designated to four groups（sham-operated group, ischemia only group, IPC ＋ sham-operated group and IPC ＋ ischemia group）. A serious loss of neuron was found in the stratum pyramidale of the hippocampal CA1 region（CA1）, not CA2/3, of the ischemia-only group at 5 days post-ischemia; however, in the IPC ＋ ischemia groups, neurons in the stratum pyramidale of the CA1 were well protected. Weak MCT4 immunoreactivity was found in the stratum pyramidale of the CA1 in the sham-operated group. MCT4 immunoreactivity in the stratum pyramidale began to decrease at 2 days post-ischemia and was hardly detected at 5 days post-ischemia; at this time point, MCT4 immunoreactivity was newly expressed in astrocytes. In the IPC ＋ sham-operated group, MCT4 immunoreactivity in the stratum pyramidale of the CA1 was increased compared with the sham-operated group, and, in the IPC ＋ ischemia group, MCT4 immunoreactivity was also increased in the stratum pyramidale compared with the ischemia only group. Briefly, present findings show that IPC apparently protected CA1 pyramidal neurons and increased or maintained MCT4 expression in the stratum pyramidale of the CA1 after transient cerebral ischemia. Our findings suggest that MCT4 appears to play a significant role in the neuroprotective mechanism of IPC in the gerbil with transient cerebral ischemia.

关键词： nerve regeneration monocarboxylate transporters ischemic preconditioning ischemia/ reperfusion injury hippocampus CA1 pyramidal neurons neural regeneration

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Pretreated Oenan the Javanica extract increases anti-inflammatory cytokines, attenuates gliosis, and protects hippocampal neurons following transient global cerebral ischemia in gerbils

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Neural Regeneration Research 2019年第9期14卷 1536-1543页

作者： Joon Ha Park In Hye Kim Ji Hyeon Ahn YooHun Noh Sung-Su Kim Tae-Kyeong Lee Jae-Chul Lee Bich-Na Shin Tae Heung Sim Hyun Sam Lee jeong hwi cho In Koo Hwang Il Jun Kang Jong Dai Kim Moo-Ho Won Department of Biomedical Science and Research Institute for Bioscience and Biotechnology Hallym UniversityChuncheonGangwonRepublic of Korea Famenity Company GwacheonGeyonggiRepublic of Korea Department of Neurobiology School of MedicineKangwon National UniversityChuncheonGangwonRepublic of Korea Danchunok Company ChuncheonGangwonRepublic of Korea Department of Histology College of Veterinary MedicineChonbuk National UniversityIksanJeollabuk.doRepublic of Korea Department of Anatomy and Cell Biology College of Veterinary Medicineand Research Institute for Veterinary ScienceSeoul National UniversitySeoulRepublic of Korea Department of Food Science and Nutrition Hallym UniversityChuncheonGangwonRepublic of Korea Division of Food Biotechnology School of BiotechnologyKangwon National UniversityChuncheonGangwonRepublic of Korea

Recently,we have reported that Oenanthe javanica extract(OJE)displays strong neuroprotective effect against ischemic damage after transient global cerebral ***,neuroprotective mechanisms of OJE have not been fully ***,this study investigated the neuroprotection of OJE in the hippocampal CA1 area and its anti-inflammatory activity in gerbils subjected to 5 minutes of transient global cerebral *** treated the animals by intragastrical injection of OJE(100 and 200 mg/kg)once daily for 1 week prior to transient global cerebral *** of OJE was observed by immunohistochemistry for neuronal nuclear antigen and histofluorescence staining for Fluoro-Jade *** of glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1 was done for astrocytosis and microgliosis,*** investigate the neuroprotective mechanisms of OJE,we performed immunohistochemistry of tumor necrosis factor-alpha and interleukin-2 for pro-inflammatory function and interleukin-4 and interleukin-13 for anti-inflammatory *** we treated the animals by intragastrical administration of 200 mg/kg of OJE,hippocampal CA1 pyramidal neurons were protected from transient global cerebral ischemia and cerebral ischemia-induced gliosis was inhibited in the ischemic hippocampal CA1 *** also found that interleukin-4 and-13 immunoreactivities were significantly increased in pyramidal neurons of the ischemic CA1 area after OJE pretreatment,and the increased immunoreactivities were sustained in the CA1 pyramidal neurons after transient global cerebral ***,OJE pretreatment did not increase interleukin-2 and tumor necrosis factor-alpha immunoreactivities in the CA1 pyramidal *** findings suggest that pretreatment with OJE can protect neurons and attenuate gliosis from transient global cerebral ischemia via increasing expressions of interleukin-4 *** experimental plan of this study was rev

关键词： Oenanthe javanica extract transient global cerebral ischemia hippocampus ischemic damage cerebral ischemia neuroprotection glial activation pro-inflammatory cytokines anti-inflammatory cytokines inflammation neural regeneration

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Delayed hippocampal neuronal death in young gerbil following transient global cerebral ischemia is related to higher and longer-term expression of p63 in the ischemic hippocampus

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Neural Regeneration Research 2015年第6期10卷 944-950页

作者： Eun Joo Bae Bai Hui Chen Bing Chun Yan Bich Na Shin jeong hwi cho In Hye Kim Ji Hyeon Ahn Jae Chul Lee Hyun-Jin Tae Seongkweon Hong Dong Won Kim Jun hwi cho Yun Lyul Lee Moo-Ho Won Joon Ha Park Department of Pediatrics Chuncheon Sacred Heart HospitalCollege of MedicineHallym University Department of Physiology College of MedicineInstitute of Neurodegeneration and NeuroregenerationHallym University Institute of Integrative Traditional & Western Medicine Medical CollegeYangzhou University Department of Neurobiology School of MedicineKangwon National University Department of Biomedical Science and Research Institute for Bioscience and Biotechnology Hallym University Department of Surgery School of MedicineKangwon National University Department of Emergency Medicine Chuncheon Sacred Heart HospitalCollege of MedicineHallym University Department of Emergency Medicine School of MedicineKangwon National University

The tumor suppressor p63 is one of p53 family members and plays a vital role as a regulator of neuronal apoptosis in the development of the nervous system. However, the role of p63 in mature neuronal death has not been addressed yet. In this study, we first compared ischemia-induced effects on p63 expression in the hippocampal regions （CA1-3） between the young and adult gerbils subjected to 5 minutes of transient global cerebral ischemia. Neuronal death in the hippocampal CA1 region of young gerbils was significantly slow compared with that in the adult gerbils after transient global cerebral ischemia, p63 immunoreactivity in the hippocampal CA1 pyramidal neurons in the sham-operated young group was significantly low compared with that in the sham-operated adult group, p63 immunoreactivity was apparently changed in ischemic hippocampal CA1 pyramidal neurons in both ischemia-operated young and adult groups. In the ischemia-operated adult groups, p63 immunoreactivity in the hippocampal CA1 pyramidal neurons was significantly decreased at 4 days post-ischemia; however, p63 immunoreactivity in the ischemia-operated young group was significantly higher than that in the ischemia-operated adult group. At 7 days post-ischemia, p63 immunoreactivity was decreased in the hippocampal CA1 pyramidal neurons in both ischemia-operated young and adult groups. Change patterns of p63 level in the hippocampal CA1 region of adult and young gerbils after ischemic damage were similar to those observed in the immunohistochemical results. These findings indicate that higher and longer-term expression of p63 in the hippocampal CA1 region of the young gerbils after ischemia/reperfusion may be related to more delayed neuronal death compared to that in the adults.

关键词： p53 tumor suppressor gene family cerebral ischemia/reperfusion pyramidal neurons CA1 region delayed neuronal death immunohistochemistry western blotting neural regeneration

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Effect of ischemic preconditioning on antioxidant status in the gerbil hippocampal CA1 region after transient forebrain ischemia

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Neural Regeneration Research 2016年第7期11卷 1081-1089页

作者： Seung Min Park Chan Woo Park Tae-Kyeong Lee jeong hwi cho Joon Ha Park Jae-Chul Lee Bai Hui Chen Bich-Na Shin Ji Hyeon Ahn Hyun-Jin Tae Myoung Cheol Shin Taek Geun Ohk Jun hwi cho Moo-Ho Won Soo Young choi In Hye Kim Department of Emergency Medicine Sacred Heart HospitalCollege of MedicineHallym University Department of Emergency Medicine School of MedicineKangwon National University Department of Neurobiology School of MedicineKangwon National University Department of Physiology College of MedicineHallym University Department of Biomedical Science Research Institute of Bioscience and BiotechnologyHallym University

Ischemic preconditioning（IPC） is a condition of sublethal transient global ischemia and exhibits neuroprotective effects against subsequent lethal ischemic ***,in this study,examined the neuroprotective effects of IPC and its effects on immunoreactive changes of antioxidant enzymes including superoxide dismutase（SOD） 1 and SOD2,catalase（CAT） and glutathione peroxidase（GPX） in the gerbil hippocampal CA1 region after transient forebrain *** neurons of the stratum pyramidale（SP） in the hippocampal CA1 region of animals died 5 days after lethal transient ischemia without IPC（8.6%（ratio of remanent neurons） of the sham-operated group）;however,IPC prevented the pyramidal neurons from subsequent lethal ischemic injury（92.3%（ratio of remanent neurons） of the sham-operated group）.SOD1,SOD2,CAT and GPX immunoreactivities in the sham-operated animals were easily detected in pyramidal neurons in the stratum pyramidale（SP） of the hippocampal CA1 region,while all of these immunoreactivities were rarely detected in the stratum pyramidale at 5 days after lethal transient ischemia without ***,their immunoreactivities in the sham-operated animals with IPC were similar to（SOD1,SOD2 and CAT） or higher（GPX） than those in the sham-operated animals without ***,their immunoreactivities in the stratum pyramidale of the ischemia-operated animals with IPC were steadily maintained after lethal ischemia/*** of western blot analysis for SOD1,SOD2,CAT and GPX were similar to immunohistochemical *** conclusion,IPC maintained or increased the expression of antioxidant enzymes in the stratum pyramidale of the hippocampal CA1 region after subsequent lethal transient forebrain ischemia and IPC exhibited neuroprotective effects in the hippocampal CA1 region against transient forebrain ischemia.

关键词： hippocampal operated antioxidant stratum subsequent superoxide glutathione neuronal hippocampus peroxidase

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