Journal
JOURNAL OF ASIAN NATURAL PRODUCTS RESEARCH
Volume 12, Issue 5, Pages 407-418Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/10286020.2010.485129
Keywords
pinocembrin; stroke; neurovascular unit; inflammation; extracellular proteolysis
Funding
- National Science and Technology Major Projects for Key New Drug Innovation [2009ZX09302-003, 2009ZX09102-057]
- Research Fund for the Doctoral Program of Higher Education of China [20091106120033]
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The purpose of the present study was to examine the protective action and mechanisms of pinocembrin (1) on the neurovascular unit (NVU) in permanent cerebral ischemic rats. Focal cerebral ischemia was induced by occlusion of middle cerebral artery (MCAO) in rats. Compound 1 (3, 10, or 30mg/kg) was intravenously injected at 0, 8, 16h after MCAO. At 24h of occlusion, 1 alleviated neuronal apoptosis, edema of astrocytic end-feet, and the deformation of endothelial cells and capillaries as revealed by the transmission electron microscopy study. To understand the mechanisms of action, the anti-inflammation effect of 1 was examined. Compound 1 reduced the expressions of tumor necrosis factor-, interleukin-1, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, inducible NO synthase and aquaporin-4; inhibited the activation of microglias and astrocytes; and downregulated the expression of matrix metalloproteinases (MMPs) in the ischemic brain. The ischemia-induced decreases in mRNA expressions of tight junction constituent proteins, occludin and ZO-1, were also inhibited by 1. These results indicated that 1 can protect the rat brain against ischemia injury by inhibiting the inflammatory cascade, reducing the expression of MMP-9, and preventing the integrity of tight junction. This resulted in the protective action of 1 on the NVU.
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