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Polyethylene glycol inhibits apoptotic cell death following traumatic spinal cord injury.
- Source :
-
Brain research [Brain Res] 2007 Jun 25; Vol. 1155, pp. 10-6. Date of Electronic Publication: 2007 May 03. - Publication Year :
- 2007
-
Abstract
- We have previously shown that local administration of polyethylene glycol (PEG, MW: 2000 Da, 50% by weight), a known membrane repair agent, immediately after trauma in guinea pig spinal cord repairs neuronal membrane disruptions and reduces oxidative injury. Here we report that a similar application of PEG resulted in marked decreases in apoptotic cell death and caspase-3 activity. We suggest that PEG may suppress apoptosis through interactions with mitochondria. This is based on our current findings that in isolated mitochondria, PEG improves mitochondrial function and reduces the release of cytochrome c, a pro-apoptotic cell death factor. This hypothesis is further supported by our previous observation that PEG enters injured cells after spinal cord injury, placing PEG in a position to directly interact with mitochondria. In summary, we conclude that PEG reduces both necrosis and apoptosis through two distinct yet synergistic pathways: repair of disrupted plasma membranes and protection of mitochondria through direct interaction.
- Subjects :
- Animals
Calcium physiology
Caspase 3 drug effects
Caspase 3 metabolism
Cell Death drug effects
Cytochromes c antagonists & inhibitors
Cytochromes c metabolism
Glutathione metabolism
Guinea Pigs
Mitochondria drug effects
Mitochondria metabolism
Polyethylene Glycols therapeutic use
Apoptosis drug effects
Polyethylene Glycols pharmacology
Spinal Cord Injuries pathology
Subjects
Details
- Language :
- English
- ISSN :
- 0006-8993
- Volume :
- 1155
- Database :
- MEDLINE
- Journal :
- Brain research
- Publication Type :
- Academic Journal
- Accession number :
- 17512912
- Full Text :
- https://doi.org/10.1016/j.brainres.2007.03.091