Role of AQP1 in the Ameliorating Effect of Electroacupuncture in a Rodent Model of Visceral Hypersensitivity.

Researchers investigated how electroacupuncture might help reduce abdominal pain and sensitivity in irritable bowel syndrome (IBS). They studied rats with IBS-like symptoms, focusing on a protein called AQP1 that appears to play a role in pain signaling. The study used 32 rats divided into four groups: normal rats, rats with IBS symptoms, rats treated with electroacupuncture at the Zusanli (ST-36) point, and rats receiving fake electroacupuncture. The IBS-like condition was created by exposing young rats to acetic acid, then testing them as adults. Results showed that rats with IBS-like symptoms had increased sensitivity to colorectal distension, along with higher levels of AQP1 protein and inflammatory markers in their intestinal tissue and nerve cells. Electroacupuncture treatment significantly reduced this hypersensitivity and lowered AQP1 expression, as well as decreased inflammatory proteins (NF-κB pathway components) and inflammatory cytokines (IL-1β and IL-18) in the blood. The fake electroacupuncture showed no such benefits. The researchers found that AQP1 is present in enteric glial cells (cells that support intestinal nerves) and small nerve cells in the spinal ganglia. By reducing AQP1 and calming inflammation, electroacupuncture appears to decrease pain sensitivity in the gut. This research suggests electroacupuncture may offer a potential treatment approach for IBS-related abdominal pain and hypersensitivity. Patients interested in acupuncture for IBS should consult with a licensed acupuncturist experienced in treating digestive conditions.

This preclinical study examined electroacupuncture's effect on visceral hypersensitivity in an acetic acid-induced IBS rodent model (n=32 male Sprague-Dawley rats across four groups). EA was administered bilaterally at ST-36, with visceral motor response assessed via electromyography during colorectal distension at 0.4, 0.8, and 1.2 ml volumes. Results demonstrated that EA significantly reduced VMR scores at higher distension volumes compared to model group. Mechanistically, EA downregulated AQP1 expression in enteric glial cells and small-diameter DRG neurons (T13-L2), inhibited NF-κB pathway activation (reduced p-p65), decreased EGC activation markers (S100β), and lowered serum IL-1β and IL-18 levels. Sham EA showed no therapeutic effect. Additional experiments with NF-κB inhibitor (PDTC) confirmed the regulatory pathway both in vivo and in LPS-activated EGC cultures in vitro. Clinical implications suggest EA may modulate visceral hypersensitivity through AQP1/NF-κB pathway inhibition, offering mechanistic support for EA treatment of IBS-related visceral pain.