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Valproic acid (VPA) impairs memory in both humans and animals, potentially by disrupting adult hippocampal neurogenesis. In contrast, baicalin-a flavonoid with antioxidant and neuroprotective properties-has demonstrated beneficial effects on brain function. The objective of this study was to assess whether baicalin, given its reported neuroprotective properties, can mitigate VPA-induced impairments in hippocampal neurogenesis and associated memory functions in adult rats. Male Sprague Dawley rats were assigned to control, VPA, baicalin, or VPA+baicalin groups. VPA (300 mg/kg) was administered intraperitoneally twice daily for 14 days; baicalin (50 mg/kg) was given once daily for 21 days. Spatial and recognition memory were assessed using the novel object location (NOL) and novel object recognition (NOR) tests. Immunofluorescent labeling with Ki-67/RECA-1, bromodeoxyuridine (BrdU), and doublecortin (DCX) was used to evaluate vascular-associated cell proliferation, cell survival, and immature neurons in the hippocampus. VPA-treated rats failed to show novelty preference in both memory tasks (p > .05) and exhibited fewer Ki-67/RECA-1-, BrdU-, and DCX-positive cells in the hippocampus (p < .05). Co-administration of baicalin significantly attenuated these deficits, improving memory performance and restoring the counts of all neurogenesis markers (p < .05). These findings suggest that baicalin may be a potential intervention to counteract VPA-induced impairments in memory and hippocampal neurogenesis in adult rats.
Yanpaisan et al. (Tue,) studied this question.