Abstract
Catalpol, an iridoid glycoside, is an isolated natural product of Rehmannia glutinosa, which has been reported to have antidiabetic properties. This study investigated
the vascular protective effects of catalpol in hyperglycemic rats with balloon-injured
carotid arteries. Balloon injury stress led to the upregulation of monocyte chemoattractant
protein-1 expression in rats with streptozotocin-induced diabetes. Western blotting
and real-time PCR were performed. In situ hybridization, immunohistochemistry, and confocal analyses were employed. Monocyte
chemoattractant protein-1 levels were increased through streptozotocin induction or
balloon injury. After treatment with catalpol, the neointimal hyperplasia area was
reduced 2 weeks after balloon injury in hyperglycemic rats. Real-time PCR and immunohistochemical
analysis demonstrated reduced levels of monocyte chemoattractant protein-1 2 weeks
after the balloon injury. Monocyte chemoattractant protein-1 expression was significantly
increased in balloon-injured rats compared with the control groups. Thus, treatment
with catalpol affected monocyte chemoattractant protein-1 expression. This study demonstrated
that catalpol downregulated monocyte chemoattractant protein-1 expression in carotid
arteries and ameliorated neointimal hyperplasia in hyperglycemic rats. The suppressive
effect of monocyte chemoattractant protein-1 suggests that it plays a key role in
neointimal hyperplasia. The results imply that catalpol is potentially effective for
preventing hyperglycemia-related ischemic cardiac diseases.
Key words
catalpol - iridoid glycoside - hyperglycemia - neointimal hyperplasia - balloon injury
- MCP-1
