View : 790 Download: 0
Short-term hyperhomocysteinemia-induced oxidative stress activates retinal glial cells and increases vascular endothelial growth factor expression in rat retina
- Title
- Short-term hyperhomocysteinemia-induced oxidative stress activates retinal glial cells and increases vascular endothelial growth factor expression in rat retina
- Authors
- Lee I.; Lee H.; Kim J.-M.; Eun H.C.; Soo J.K.; Chang N.
- Ewha Authors
- 장남수; 이화영
- SCOPUS Author ID
- 장남수; 이화영
- Issue Date
- 2007
- Journal Title
- Bioscience, Biotechnology and Biochemistry
- ISSN
- 0916-8451
- Citation
- Bioscience, Biotechnology and Biochemistry vol. 71, no. 5, pp. 1203 - 1210
- Indexed
- SCI; SCIE; SCOPUS
- Document Type
- Article
- Abstract
- Hyperhomocysteinemia is associated with an increase in the incidence of vascular diseases, including retinal vascular diseases. We examined the effects of high plasma levels of homocysteine on retinal glial cells and vascular endothelial growth factor (VEGF) expression. Male Sprague-Dawley rats were fed either a 3.0 g/kg homocystine diet or a control diet for 2 week. The homocystine-diet group had higher plasma levels of homocysteine and thiobarbituric acid reactive substances (TBARSs) and lower plasma levels of folate, retinol, α-tocopherol, and retinal expression of CuZn superoxide dismutase (SOD) than the controls. The rats fed the homocystine-diet showed an increase in vimentin, glial fibrillary acidic protein (GFAP), and VEGF immunoreactivity in the retina as compared to the controls. The increase in vimentin immunoreactivity in the hyperhomocysteinemic rats was correlated with changes in GFAP immunoreactivity in astrocytes within the ganglion cell layer. We found for the first time that short-term hyperhomocysteinemia-induced oxidative stress activates retinal glial cells and increases VEGF expression in the retina.
- DOI
- 10.1271/bbb.60657
- Appears in Collections:
- 신산업융합대학 > 식품영양학과 > Journal papers
- Files in This Item:
There are no files associated with this item.
- Export
- RIS (EndNote)
- XLS (Excel)
- XML