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Serum Metabolomics in the Rat Model of Recurrent Pelvic Pain

ABSTRACT:

This study aimed to investigate systemic metabolic alterations underlying pain-depression comorbidity in the Recurrent Pelvic Pain (RPP) rat model using untargeted serum metabolomics (UPLC-Q-Orbitrap-MS). Comparative analysis revealed distinct metabolic profiles, identifying 234 differential metabolites enriched in steroids, fatty acyls, and carboxylic acids. KEGG analysis highlighted reprogramming of amino acid metabolism (e.g., phenylalanine, tyrosine, and tryptophan biosynthesis) and arachidonic acid metabolism. Integrative target prediction identified 10 key overlapping targets (e.g., TRPV1, OPRM1, PTGS2) associated with inflammatory response, fatty acid metabolism, and synaptic signaling. These targets were further linked to chronic pain and hyperalgesia. The metabolomic profile supports progressive nociceptive sensitization and reveals altered neurotransmitter biosynthesis pathways, providing insight into mechanisms of pain-depression comorbidity and potential therapeutic targets.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse-phase, Liquid Chromatography MS - positive - reverse-phase

PROVIDER: MTBLS13869 | MetaboLights | 2026-02-11

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS13869_LC-MS_negative_reverse-phase_metabolite_profiling.txt	Txt
	a_MTBLS13869_LC-MS_positive_reverse-phase_metabolite_profiling.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS13869_LC-MS_negative_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular
	m_MTBLS13869_LC-MS_positive_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular

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Project description:Neuropathic pain is a chronic debilitating condition with a high comorbidity with depression. Clinical reports and animal studies have suggested that both the medial prefrontal cortex (mPFC) and the anterior cingulate cortex (ACC) are critically implicated in regulating the affective symptoms of neuropathic pain. Neuropathic pain induces long-term structural, functional and biochemical changes in both regions, which are thought to be regulated by multiple waves of gene transcription. However, the similarity and differences in the transcriptomic profiles changed by neuropathic pain between these regions are largely unknown. Furthermore, women are more susceptible to pain and depression than men. The molecular mechanisms underlying this sexual dimorphism remain to be explored. Here, we performed RNA sequencing and analyzed the transcriptomic profiles of the mPFC and ACC of female and male mice at 2 weeks after spared nerve injury (SNI), an early time point when the mice began to show mild depressive symptoms. Our results show that the SNI-induced transcriptomic changes in female and male mice are largely distinct. Interestingly, the female mice exhibit more robust transcriptomic changes in the ACC than male, whereas the opposite pattern occurs in the mPFC. Cell type enrichment analyses reveal that the differentially expressed genes involve genes enriched in both neurons and various types of glia. We further performed Gene Set Enrichment Analysis (GSEA), which reveal significant de-enrichment of myelin sheath development in both female and male mPFC after SNI. In the female ACC, gene sets for synaptic organization and mitochondria function are enriched, and gene sets for extracellular matrix are de-enriched after SNI, while such signatures are absent in male ACC. Collectively, these findings reveal sexual dimorphism at the transcriptional level induced by neuropathic pain, and provide novel therapeutic targets for chronic pain and its associated affective disorders.

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Serum Metabolomics in the Rat Model of Recurrent Pelvic Pain

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