Baicalin counteracts valproic acid-induced memory impairment by restoring neurogenesis in the hippocampus of adult rats.

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.