We recently reported the protective effects of
chlorogenic acid (CGA) in a transient
middle cerebral artery occlusion (tMCAo) rat model. The current study further investigated the protective effects of the metabolites of CGA and
dihydrocaffeic acid (DHCA) was selected for further study after screening using the same tMCAo rat model. In the current study, tMCAo rats (2 h of MCAo followed by 22 h of reperfusion) were injected with various doses of DHCA at 0 and 2 h after onset of
ischemia. We assessed brain damage, functional deficits,
brain edema, and blood-brain barrier damage at 24 h after
ischemia. For investigating the mechanism, in vitro zymography and western blotting analysis were performed to determine the expression and activation of
matrix metalloproteinase (MMP)-2 and -9. DHCA (3, 10, and 30 mg/kg, i.p.) dose-dependently reduced
brain infarct volume, behavioral deficits, brain water content, and
Evans Blue (EB) leakage. DHCA inhibited expression and activation of MMP-2 and MMP-9. Therefore, DHCA might be one of the important metabolites of CGA and of natural products, including
coffee, with protective effects on
ischemia-induced neuronal damage and
brain edema.