Objective: The pathophysiological mechanism of global ischemia damage is complex. Recent studies indicate that the excessive inflammatory response induced by cerebral ischemia/reperfusion plays an important role in ischemic damage. Baicalin (5,6-dihydroxy-7-O-glucuronide flavonoid glycosides) is extracted from the dry dicotyledonous skullcap root, and belongs to one of the flavonoid compounds. Baicalin has a neuroprotective effect in a variety of brain injury animal models, although the mechanism remains unclear. We suggest that baicalin prevents deterioration in rats' spatial learning abilities associated with acute global cerebral ischemia by inhibiting the inflammatory reaction and reducing apoptosis.
Methods: Forty-two Sprague Dawley rats were divided into three groups: 14 rats in a sham (S) group; 14 in a global cerebral ischemia/reperfusion (I/R) group; and 14 in a global cerebral ischemia/reperfusion+baicalin treatment (I/RB) group. A Morris water maze test was used to assess learning and memory, HE staining was conducted for pathomorphology, a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay was used to determine neuronal apoptosis, and Western blot for cyclooxygenase-2 (COX-2) expression in the hippocampus CA1 region.
Results: Compared to the I/R group, Baicalin improved the learning and memory of I/RB rats. There was decreased hippocampal apoptosis and a reduction in the level of COX-2 expression in the I/RB group. In addition, the pathomorphological changes were worse in the I/R than in the I/RB group.
Conclusion: Baicalin improved the detrimental effects on spatial memory associated with global cerebral ischemia by reducing hippocampal apoptosis via the inhibition of COX-2 expression.
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