Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1196104 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31656474.fastq.gz | Fastqsanger.gz | |||
| SRR31656475.fastq.gz | Fastqsanger.gz | |||
| SRR31656476.fastq.gz | Fastqsanger.gz | |||
| SRR31656477.fastq.gz | Fastqsanger.gz |
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Project description:This study investigated whether dietary poricoic acid A (PAA) alleviates chronic unpredictable stress (CUS)-induced depressive-like behaviors in mice by modulating the gut microbiota-immune axis. Male C57BL/6J mice were subjected to CUS and treated with PAA. Results showed that PAA alleviated depressive- and anxiety-like behaviors, reduced hippocampal neuronal damage, and restored gut microbiota composition by suppressing harmful bacteria like Ligilactobacillus murinus while promoting beneficial taxa such as Akkermansia muciniphila and Lactobacillus reuteri. Hippocampal transcriptomics revealed that PAA modulated immune cell infiltration by reducing M1 and restoring M2 macrophages, with significant correlations between gut microbial taxa and hippocampal immune gene expression. Functional analyses indicated that PAA regulated pathways related to synaptic plasticity and neuroinflammation, which was confirmed by qPCR and Western blot showing restored expression of HSP90B1, RPS6KB2, IGF2BP2, and COL4A5. In conclusion, dietary PAA alleviates depressive-like behaviors in CUS mice by remodeling the gut microbiota and modulating the hippocampal M1/M2 macrophage balance via the gut-brain axis, supporting its potential as a prebiotic-like nutritional agent for major depressive disorder.
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Project description:Depression is associated with neuroinflammation and microglial activation. This study investigated the effects of sedanolide in an LPS-induced mouse model of depressive-like behaviors. RNA sequencing of medial prefrontal cortex (mPFC) tissues was performed to identify transcriptomic changes associated with sedanolide treatment. Differential expression analysis revealed candidate genes involved in inflammatory pathways, including C3 and MMP9. Further validation demonstrated that sedanolide regulates neuroinflammation and microglial metabolic reprogramming through the C3a/C3aR signaling axis.
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Project description:Background: Perinatal depression is a prevalent disorder with detrimental effects on both maternal mental health and offspring neurodevelopment. Neuroinflammation mediated by microglial polarization is implicated in its pathogenesis. Oridonin, a natural diterpenoid with anti-inflammatory properties, has shown potential in various disease models, but its efficacy in perinatal depression and its intergenerational impacts remain unexplored. Methods: A mouse model of chronic variable stress (CVS) during lactation was established. Depressive-like behaviors were assessed using the sucrose preference test (SPT), forced swim test (FST), and novelty-suppressed feeding test (NSFT). Stressed dams were randomly assigned to receive daily intraperitoneal injections of oridonin (10 mg/kg), fluoxetine (10 mg/kg), or vehicle for 14 days. Maternal prefrontal cortex (PFC) was analyzed for microglial polarization (via Iba1, iNOS, CD206 immunofluorescence) and cytokine profiles (via Western blot). The offspring's prefrontal cortex and hippocampus were subjected to single-cell RNA sequencing (scRNA-seq) to delineate cell-type-specific transcriptional responses. Results: CVS induced significant depressive-like behaviors in dams, promoted M1 microglial polarization, increased pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), and decreased anti-inflammatory cytokines (IL-4, IL-10, IL-13) in the PFC. Oridonin treatment ameliorated these behavioral deficits, suppressed M1 polarization, enhanced M2 polarization, and normalized cytokine levels, comparable to fluoxetine. scRNA-seq of offspring revealed that oridonin, but not fluoxetine, induced extensive, region-specific transcriptomic reprogramming. Notably, oridonin elicited 220 differentially expressed genes (DEGs) in hippocampal oligodendrocytes, impacted neural circuit-related pathways, and promoted a transcriptional signature associated with synaptic stabilization in the hippocampus while modulating metabolic and stress-response pathways in the prefrontal cortex. Conclusion: Oridonin alleviates maternal depressive-like behaviors by driving microglial polarization toward an anti-inflammatory M2 phenotype and suppressing neuroinflammation. Crucially, maternal oridonin treatment during lactation induces robust, region-specific transcriptional changes in the offspring brain, suggesting a profound intergenerational programming effect. Our findings highlight oridonin's potential as a multi-target therapeutic agent for perinatal depression and its long-lasting impact on offspring neurodevelopment.
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Project description:Stress is a known risk factor of major depressive disorder (MDD). T cell-restricted intracellular antigen 1 (TIA1), an RNA-binding protein, regulates mRNA stability and functions as a translational silencer under stress. However, its roles in MDD remain unclear. Here, we found that TIA1 was mainly expressed in neurons and significantly downregulated in the hippocampus of depressive-like mice after chronic unpredictable mild stress (CUMS) or lipopolysaccharide (LPS) induction. Interestingly, conditional knockout of TIA1 in the central nervous system (CNS) (TIA1Nestin-CKO mice) aggravated the depressive-like behaviors after LPS or CUMS exposure. Further analysis revealed that TIA1 was mainly expressed in CaMKIIα+ neurons, and its knockout in CaMKIIα+ neurons of ventral hippocampal CA1 (vCA1), but not in astrocytes, aggravated depressive-like behaviors after LPS or CUMS induction. Moreover, synaptic transmission was disrupted in these TIA1-deficiency mice after LPS induction. Mechanistically, Cacna2d1 (a well-known gene associated with depression) was a key TIA1 target based on results of RNA immunoprecipitation sequencing (RIP-Seq) and single-nucleus RNA sequencing (snRNA-seq) in MDD patients. TIA1 bound to Cacna2d1 mRNA and downregulated its expression in neuronal cells. In contrast, in TIA1CaMKIIα-CKO mice, Cacna2d1 was upregulated in vCA1 neurons, aggravated the depressive-like behaviors. Finally, both chemogenetic activation of excitatory neurons in the vCA1 or pharmacological inhibition of Cacna2d1 effectively rescued the aggravation of depressive-like behaviors. Together, these results reveal a previously unrecognized role of excitatory neuronal TIA1 in vCA1 by suppressing Cacna2d1, which advances our understanding of the molecular mechanism underlying stress-induced depressive symptoms.
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Project description:Dietary Poricoic acid A alleviates depressive-like behaviors by targeting the gut microbiota-immune axis
| PRJNA1452981 | ENA