ArticleAdvances in pharmacological and pharmaceutical sciences2025
Regulation of Cerebral BDNF, VEGF, and GluN2B Gene Expression and Cytokine Levels by Riparin A in a Murine Model of Depression.
Article in Advances in pharmacological and pharmaceutical sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Regulation of Cerebral BDNF, VEGF, and GluN2B Gene Expression and Cytokine Levels by Riparin A in a Murine Model of Depression.Advances in pharmacological and pharmaceutical sciences · 2025Article
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5 authors.
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Abstract
Riparin A is a synthetic compound with established antidepressant and anxiolytic properties. Given its therapeutic potential and the crucial roles of brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF), and the GluN2B subunit of the N-methyl-D-aspartate (NMDA) receptor in the pathophysiology and treatment of depression, this study aimed to evaluate the effects of Riparin A on the expression of these neurotrophic factors and receptor subunit in the hippocampus and cortex of rats subjected to the chronic unpredictable mild stress (CUMS) model of depression. Using RT-qPCR, we observed that Riparin A significantly upregulated BDNF and VEGF mRNA levels while downregulating GluN2B expression, remarkably on the hippocampal area. Furthermore, ELISA assays revealed that Riparin A modulated neuroinflammation by reducing proinflammatory cytokines TNF-α and IL-1β while increasing anti-inflammatory cytokines IL-4 and IL-10. These findings support the antidepressant properties of Riparin A and shed light on its underlying mechanisms, reinforcing the interplay between neurotrophic and inflammatory pathways in pathophysiology of depression and its treatment.
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