Neurogastroenterology and motility · 2025
Revealing the Immune and Inflammatory Mechanisms of Electroacupuncture in Male IBS Rats Through Multi-Omics Analysis.
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Wang Lijun, Chang Xiaoli, Zhang Lili, Xu Ruijian, Chen Ling, Chen Shaozong, Yang Zongbao
Аннотация
BACKGROUND: Electroacupuncture (EA) therapy shows promising efficacy in irritable bowel syndrome (IBS). This study integrated nontargeted metabolomics with transcriptomics to investigate the immune-inflammatory mechanisms underlying the effects of EA therapy in male IBS rats.
METHOD: IBS was induced in rats using water avoidance stress (WAS), and EA was applied at ST25 and BL25 acupoints. The IBS model was evaluated alongside assessments of depressive behavior. Visceral sensation was quantified using the abdominal withdrawal reflex (AWR) and the area under the EMG curve of abdominorectal muscles. The intestinal barrier integrity was analyzed by measuring ZO-1 and MUC2 levels, while inflammation was assessed through IL-1β and TNF-α measurements. Colon samples underwent nontarget metabolomics and transcriptomics analyses, and DEGs were validated using RT-PCR and WB to identify potential pathways. Networks of DEGs and differential metabolites were subsequently constructed to elucidate their interactions.
RESULT: EA treatment increased the expression of ZO-1 and MUC2, inhibited the IL-1β and TNF-α, and alleviated visceral hypersensitivity and depressive behavior. Transcriptomics identified 13 DEGs, indicating that EA modified the gene expression levels of Lck, Cd28, Il16, Nfatc2, Ccl17, Pik3cd, Zap70, Lat, Cd40, Cxcl10, Tlr9, Tnfsf8, and Tnfsf11. The underlying mechanism may involve the inhibition of PD-1/PD-L1, TCR and NF-κB signaling pathways. Metabolomics identified 14 differential metabolites, suggesting that EA may correct metabolic disturbances.
CONCLUSION: EA alleviates intestinal damage, inflammation, and behavioral symptoms in male IBS rats, potentially through modulation of immune-inflammatory pathways and metabolic homeostasis. This study focused on male rats; future research including females may clarify sex-related differences in EA.
METHOD: IBS was induced in rats using water avoidance stress (WAS), and EA was applied at ST25 and BL25 acupoints. The IBS model was evaluated alongside assessments of depressive behavior. Visceral sensation was quantified using the abdominal withdrawal reflex (AWR) and the area under the EMG curve of abdominorectal muscles. The intestinal barrier integrity was analyzed by measuring ZO-1 and MUC2 levels, while inflammation was assessed through IL-1β and TNF-α measurements. Colon samples underwent nontarget metabolomics and transcriptomics analyses, and DEGs were validated using RT-PCR and WB to identify potential pathways. Networks of DEGs and differential metabolites were subsequently constructed to elucidate their interactions.
RESULT: EA treatment increased the expression of ZO-1 and MUC2, inhibited the IL-1β and TNF-α, and alleviated visceral hypersensitivity and depressive behavior. Transcriptomics identified 13 DEGs, indicating that EA modified the gene expression levels of Lck, Cd28, Il16, Nfatc2, Ccl17, Pik3cd, Zap70, Lat, Cd40, Cxcl10, Tlr9, Tnfsf8, and Tnfsf11. The underlying mechanism may involve the inhibition of PD-1/PD-L1, TCR and NF-κB signaling pathways. Metabolomics identified 14 differential metabolites, suggesting that EA may correct metabolic disturbances.
CONCLUSION: EA alleviates intestinal damage, inflammation, and behavioral symptoms in male IBS rats, potentially through modulation of immune-inflammatory pathways and metabolic homeostasis. This study focused on male rats; future research including females may clarify sex-related differences in EA.