Abstract
Objective
This study aimed to explore the mechanisms by which electroacupuncture (EA) treats irritable bowel syndrome (IBS) in rats.
Materials and Methods
Forty pups born to three healthy Specific Pathogen Free-grade SD rats were used, of which ten were selected as the control group (CG). The remaining thirty pups were prepared into the IBS model and grouped into the IBS model group (IBSG), ketotifen (KT) group (KTG), EA group (EAG), with interventions conducted once daily for 14 d. Anxiety-like behavior in rats was assessed, diarrhea symptoms were examined, and visceral hypersensitivity (VHS) was evaluated. Substance P (SP), protease-activated receptor-2 (PAR-2), and serotonin (5-HT) levels were detected.
Results
Compared with the CG, the IBSG suggested reduced movement distance, rearing frequency, and time spent in the central area; increased fecal water content (WC) and diarrhea index (DI); increased abdominal withdrawal reflex (AWR) scores under 20, 40, 60, and 80 mmHg pressures; decreased colonic pain threshold (PT) and slow-wave (SW) frequency; increased serum SP, PAR-2, and 5-HT; and increased protein expression levels of TLR4, NF-κB, and NLRP3 in colon tissues (P < 0.05). Compared with the IBSG, the KTG and EAG suggested increased movement distance, rearing frequency, and time spent in the central area; decreased fecal WC and DI; decreased AWR scores; increased colonic PT and SW frequency; decreased serum SP, PAR-2, and 5-HT; and reduced TLR4, NF-κB, and NLRP3 in the colon (P < 0.05).
Conclusion
The comprehensive EA intervention targeting “Tianshu” (ST25), “Zusanli” (ST36), and “Shangjuxu” (ST37) was associated with alleviated VHS, reduced markers of low-grade colonic inflammation, and improved colonic function in rats with IBS. These effects were consistent with the downregulation of the TLR4/NF-κB/NLRP3 signaling pathway.
Keywords
Get full access to this article
View all access options for this article.
References
Supplementary Material
Please find the following supplemental material available below.
For Open Access articles published under a Creative Commons License, all supplemental material carries the same license as the article it is associated with.
For non-Open Access articles published, all supplemental material carries a non-exclusive license, and permission requests for re-use of supplemental material or any part of supplemental material shall be sent directly to the copyright owner as specified in the copyright notice associated with the article.
