NDLI: Neuroprotective Effects of PEP-1-Cu,Zn-SOD against Ischemic Neuronal Damage in the Rabbit Spinal Cord

Content Provider	Springer Nature Link
Author	Kim, Woosuk Kim, Dae Won Yoo, Dae Young Chung, Jin Young Hwang, In Koo Won, Moo Ho Choi, Soo Young Jeon, Sei Woong Jeong, Je Hoon Hwang, Hyung Sik Moon, Seung Myung
Copyright Year	2011
Abstract	A rabbit model of spinal cord ischemia has been introduced as a good model to investigate the pathophysiology of ischemia–reperfusion (I–R)-induced paraplegia. In the present study, we observed the effects of Cu,Zn-superoxide dismutase (SOD1) against ischemic damage in the ventral horn of L$_{5–6}$ levels in the rabbit spinal cord. For this study, the expression vector PEP-1 was constructed, and this vector was fused with SOD1 to create a PEP-1-SOD1 fusion protein that easily penetrated the blood–brain barrier. Spinal cord ischemia was induced by transient occlusion of the abdominal aorta for 15 min. PEP-1-SOD1 (0.5 mg/kg) was intraperitoneally administered to rabbits 30 min before ischemic surgery. The administration of PEP-1-SOD1 significantly improved neurological scores compared to those in the PEP-1 (vehicle)-treated ischemia group. Also, in this group, the number of cresyl violet-positive cells at 72 h after I–R was much higher than that in the vehicle-treated ischemia group. Malondialdehyde levels were significantly decreased in the ischemic spinal cord of the PEP-1-SOD1-treated ischemia group compared to those in the vehicle-treated ischemia group. In contrast, the administration of PEP-1-SOD1 significantly ameliorated the ischemia–induced reduction of SOD and catalase levels in the ischemic spinal cord. These results suggest that PEP-1-SOD1 protects neurons from spinal ischemic damage by decreasing lipid peroxidation and maintaining SOD and catalase levels in the ischemic rabbit spinal cord.
Starting Page	307
Ending Page	313
Page Count	7
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	37
Issue Number	2
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2011-10-02
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Transient spinal ischemia Neuroprotection Lipid peroxidation Antioxidants Cell Biology Neurosciences Neurochemistry Biochemistry Neurology
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Heme Oxygenase-1 Protects Neurons from Ischemic Damage by Upregulating Expression of Cu,Zn-Superoxide Dismutase, Catalase, and Brain-Derived Neurotrophic Factor in the Rabbit Spinal Cord

Tat-DJ-1 Protects Neurons from Ischemic Damage in the Ventral Horn of Rabbit Spinal Cord Via Increasing Antioxidant Levels

Cu, Zn-Superoxide Dismutase Increases the Therapeutic Potential of Adipose-derived Mesenchymal Stem Cells by Maintaining Antioxidant Enzyme Levels

Commentary of “Copper Chaperone for Cu,Zn-SOD supplement potentiates the Cu,Zn- SOD function of neuroprotective effects against ischemic neuronal damage in the gerbil hippocampus”

Antioxidant, Anticonvulsive and Neuroprotective Effects of Dapsone and Phenobarbital Against Kainic Acid-Induced Damage in Rats

Extract from Terminalia chebula Seeds Protect Against Experimental Ischemic Neuronal Damage Via Maintaining SODs and BDNF Levels

Repeated Administration of PEP-1-Cu,Zn-Superoxide Dismutase and PEP-1-Peroxiredoxin-2 to Senescent Mice Induced by d-galactose Improves the Hippocampal Functions

Increases of Catalase and Glutathione Peroxidase Expressions by Lacosamide Pretreatment Contributes to Neuroprotection Against Experimentally Induced Transient Cerebral Ischemia

Neuroprotective Evaluation of Tilia americana and Annona diversifolia in the Neuronal Damage Induced by Intestinal Ischemia

Neuroprotective Effects of PEP-1-Cu,Zn-SOD against Ischemic Neuronal Damage in the Rabbit Spinal Cord

Similar Documents

Heme Oxygenase-1 Protects Neurons from Ischemic Damage by Upregulating Expression of Cu,Zn-Superoxide Dismutase, Catalase, and Brain-Derived Neurotrophic Factor in the Rabbit Spinal Cord

Tat-DJ-1 Protects Neurons from Ischemic Damage in the Ventral Horn of Rabbit Spinal Cord Via Increasing Antioxidant Levels

Cu, Zn-Superoxide Dismutase Increases the Therapeutic Potential of Adipose-derived Mesenchymal Stem Cells by Maintaining Antioxidant Enzyme Levels

Commentary of “Copper Chaperone for Cu,Zn-SOD supplement potentiates the Cu,Zn- SOD function of neuroprotective effects against ischemic neuronal damage in the gerbil hippocampus”

Antioxidant, Anticonvulsive and Neuroprotective Effects of Dapsone and Phenobarbital Against Kainic Acid-Induced Damage in Rats

Extract from Terminalia chebula Seeds Protect Against Experimental Ischemic Neuronal Damage Via Maintaining SODs and BDNF Levels

Repeated Administration of PEP-1-Cu,Zn-Superoxide Dismutase and PEP-1-Peroxiredoxin-2 to Senescent Mice Induced by d-galactose Improves the Hippocampal Functions

Increases of Catalase and Glutathione Peroxidase Expressions by Lacosamide Pretreatment Contributes to Neuroprotection Against Experimentally Induced Transient Cerebral Ischemia

Neuroprotective Evaluation of Tilia americana and Annona diversifolia in the Neuronal Damage Induced by Intestinal Ischemia

Neuroprotective Effects of PEP-1-Cu,Zn-SOD against Ischemic Neuronal Damage in the Rabbit Spinal Cord