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Background <p>Aquaporins 1 (AQP1), the first water channel protein, is involved in central and peripheral nociception. However, it remains unclear whether AQP1 contributes to visceral hypersensitivity. We hypothesize that AQP1 contributes to acetic acid-induced visceral hypersensitivity in a rat model of irritable bowel syndrome (IBS) and that electroacupuncture (EA) improves visceral hypersensitivity by down-regulating the expression of AQP1 in enteric glial cells (EGCs) and dorsal root ganglion (DRG).</p> Methods <p>Animal experiments were conducted in two batches, the first batch consisted of 32 male Sprague–Dawley rats were randomly divided into four groups: control, model, EA, and sham EA. The IBS model was established by acetic acid enema in neonatal rats, and the experiments were conducted after they reached adulthood. The rats were placed with one pair of electrodes at the external oblique muscles for electromyogram (EMG) recording, and visceral sensitivity during colorectal distension (CRD) with 0.4, 0.8, and 1.2&#xa0;ml of injected water was assessed. The rats' bilateral Zusanli acupoints (ST-36) were used for electroacupuncture (EA). The expressions of AQP1, EGC activation markers (S100β), and NF-κB in colonic tissues and DRG were assessed by real-time PCR, Western blot, and immunofluorescence. ELISA was used to measure the amounts of IL-1β and IL-18 in the serum. In the second batch, twenty-four rats were randomly divided into three groups: control, model, NF-κB inhibitor group (PDTC group), and similarly performed VMR, AQP1 expression assays to verify the regulatory effect of NF-κB pathway on AQP1 and EGC in vivo. Meanwhile, enteric glial cells were cultured in vitro and activated with lipopolysaccharide (LPS), NF-κB inhibitor intervention; real-time PCR and Western blot were performed to detect the expression of AQP1 and S100β to confirm the effect of NF-κB pathway on AQP1 in vitro.</p> Results <p>At 0.8&#xa0;ml and 1.2&#xa0;ml expansion volumes, visceral sensitivity was significantly increased in the model group, and electroacupuncture reversed this change, with no such effect in the sham electroacupuncture (sham EA) group. In the colon, AQP1 colocalizes with S100β, and compared with the control group, the protein expression of AQP1, phosphorylated nuclear factor kappa B p65 (p-p65), S100β in the colon, and the serum levels of IL‐1β and IL‐18 were markedly increased of the model group; electroacupuncture decreased VMR score, the serum levels of IL‐1β and IL‐18, and downregulated the protein expression of AQP1, p-p65, S100β, whereas sham EA group showed no such changes. In the dorsal root ganglion (T13-L2), AQP1 was mainly expressed in neurons with a smaller diameter, and the changing trend of AQP1, p-p65 in each group was consistent with that in the colon. In addition, AQP1 expression was downregulated in EGC after NF-κB inhibitor (PDTC) treatment both in vivo and in vitro.</p> Conclusion <p>EA ameliorates visceral hypersensitivity in a rodent model of IBS by down-regulating AQP1 expression and inhibiting the NF-κB pathway and may have a therapeutic potential in the treatment of visceral hypersensitivity.</p>

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

  • 期刊论文

  • 发表日期：

    2025年8月5日

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  • Laifu Li,
  • Lijuan Xu,
  • Lianli Wang,
  • Yating Sun,
  • Yan Ran,
  • Lin Mei,
  • Yan Zhuang,
  • Xinping Zhang,
  • Fangchen Ye,
  • Fei Dai

摘要

Background

Aquaporins 1 (AQP1), the first water channel protein, is involved in central and peripheral nociception. However, it remains unclear whether AQP1 contributes to visceral hypersensitivity. We hypothesize that AQP1 contributes to acetic acid-induced visceral hypersensitivity in a rat model of irritable bowel syndrome (IBS) and that electroacupuncture (EA) improves visceral hypersensitivity by down-regulating the expression of AQP1 in enteric glial cells (EGCs) and dorsal root ganglion (DRG).

Methods

Animal experiments were conducted in two batches, the first batch consisted of 32 male Sprague–Dawley rats were randomly divided into four groups: control, model, EA, and sham EA. The IBS model was established by acetic acid enema in neonatal rats, and the experiments were conducted after they reached adulthood. The rats were placed with one pair of electrodes at the external oblique muscles for electromyogram (EMG) recording, and visceral sensitivity during colorectal distension (CRD) with 0.4, 0.8, and 1.2 ml of injected water was assessed. The rats' bilateral Zusanli acupoints (ST-36) were used for electroacupuncture (EA). The expressions of AQP1, EGC activation markers (S100β), and NF-κB in colonic tissues and DRG were assessed by real-time PCR, Western blot, and immunofluorescence. ELISA was used to measure the amounts of IL-1β and IL-18 in the serum. In the second batch, twenty-four rats were randomly divided into three groups: control, model, NF-κB inhibitor group (PDTC group), and similarly performed VMR, AQP1 expression assays to verify the regulatory effect of NF-κB pathway on AQP1 and EGC in vivo. Meanwhile, enteric glial cells were cultured in vitro and activated with lipopolysaccharide (LPS), NF-κB inhibitor intervention; real-time PCR and Western blot were performed to detect the expression of AQP1 and S100β to confirm the effect of NF-κB pathway on AQP1 in vitro.

Results

At 0.8 ml and 1.2 ml expansion volumes, visceral sensitivity was significantly increased in the model group, and electroacupuncture reversed this change, with no such effect in the sham electroacupuncture (sham EA) group. In the colon, AQP1 colocalizes with S100β, and compared with the control group, the protein expression of AQP1, phosphorylated nuclear factor kappa B p65 (p-p65), S100β in the colon, and the serum levels of IL‐1β and IL‐18 were markedly increased of the model group; electroacupuncture decreased VMR score, the serum levels of IL‐1β and IL‐18, and downregulated the protein expression of AQP1, p-p65, S100β, whereas sham EA group showed no such changes. In the dorsal root ganglion (T13-L2), AQP1 was mainly expressed in neurons with a smaller diameter, and the changing trend of AQP1, p-p65 in each group was consistent with that in the colon. In addition, AQP1 expression was downregulated in EGC after NF-κB inhibitor (PDTC) treatment both in vivo and in vitro.

Conclusion

EA ameliorates visceral hypersensitivity in a rodent model of IBS by down-regulating AQP1 expression and inhibiting the NF-κB pathway and may have a therapeutic potential in the treatment of visceral hypersensitivity.