Electroacupuncture at Baliao Points Attenuates Visceral Hypersensitivity in Irritable Bowel Syndrome via Gut-Microbiota-Mast Cell-TPRV1 Axis Modulation.

BACKGROUND

Visceral hypersensitivity (VH) is a key pathophysiological feature of irritable bowel syndrome (IBS), contributing to chronic abdominal pain and discomfort. While electroacupuncture (EA) has demonstrated efficacy in alleviating IBS symptoms, the mechanisms underlying its effects at the Baliao acupoint remain unclear.

METHODS

In this translational study, we enrolled 40 IBS patients (gender-balanced, aged 30-60 years) who received standardized EA treatment at Baliao acupoints, with pain intensity assessed using visual analogue scale (VAS) scoring. An IBS rat model was established using acetic acid enema combined with restraint stress. Rats received EA at Baliao or sham acupuncture for 2 weeks. Visceral sensitivity was assessed via abdominal withdrawal reflex (AWR), while mast cell (MC) numbers, histamine and substance P (SP) release, and tight junction proteins (ZO-1, occludin) were quantified. Gut-microbiota composition was analyzed by 16S rDNA sequencing, and the alterations of TRPV1+ neuron and MAPK signaling were evaluated via immunofluorescence and Western blot.

RESULTS

EA at Baliao significantly attenuated VH in both IBS patients (reduced VAS scores, difference -3.000 ± 0.4264) and rats (lower AWR scores, difference 1.050 ± 0.2630), compared to the sham group. Treatment with EA restored gut microbial diversity, promoting beneficial taxa (Bifidobacterium, Akkermansia) while suppressing pathobionts (Helicobacter, Prevotella). Moreover, EA inhibited MC degranulation, reducing histamine (↓40%, p < 0.01) and SP (↓28%, p < 0.05), and enhanced intestinal barrier integrity via ZO-1/occludin upregulation. Crucially, EA suppressed TRPV1+ neuron activation in the colon and dorsal root ganglia, disrupting MC-neuron crosstalk through TRPV1/MAPK pathway modulation.

CONCLUSION

EA (Baliao) alleviates VH by modulating gut microbiota, inhibiting MC activation, and blocking TRPV1 positive neuron mediated signal transmission. These findings highlight its potential as a non-pharmacological therapy for IBS, targeting multiple pathological axes.