# LIPUS Enhances Gallbladder Motility via ANO1 in Acute Cholecystitis Guinea Pigs

## TL;DR

Low-intensity pulsed ultrasound improves gallbladder function in inflamed guinea pigs by boosting muscle contractions and reducing inflammation.

## Contribution

LIPUS is shown to enhance gallbladder motility via ANO1 activation in ICCs during acute cholecystitis.

## Key findings

- LIPUS increased intracellular Ca2+ by activating the Ano1 channel in ICCs.
- LIPUS improved gallbladder muscle tone by 71.3% and reduced inflammation scores by 40.7%.
- LIPUS promotes ICC recovery and reduces inflammation in acute cholecystitis.

## Abstract

Background: Acute cholecystitis (AC) is characterized by gallbladder inflammation and is commonly accompanied by disordered gallbladder motility. Although laparoscopic cholecystectomy is the standard treatment, it carries procedure-related risks. Low-intensity pulsed ultrasound (LIPUS), a safe and noninvasive modality widely applied for muscle repair, may offer therapeutic benefits for AC-associated motility dysfunction. Methods: In vivo, LIPUS (0.5 W/cm2) was applied for 15 min daily to acute cholecystitis guinea pigs over three consecutive days, starting 24 h after reversing common bile duct ligation (CBDL) surgery. In vitro, LIPUS (0.5 W/cm2) was delivered for 5 min to isolated gallbladder muscle strips and for 30 s to isolated interstitial cells of Cajal (ICCs). Gallbladder function and histology were assessed in vitro and in vivo using immunofluorescence, Western blotting, calcium imaging, muscle strip contractility testing, and related molecular methods. Results: LIPUS increased intracellular Ca2+ by activating the Ano1 channel in ICCs, thereby enhancing gallbladder smooth muscle contractility. At 72 h, the LIPUS 72 h (+) group showed a 71.3% increase in gallbladder muscle tone (p = 0.0001) and a 40.7% reduction in inflammation scores (p = 0.0001) compared with the LIPUS 72 h (−) group. Conclusions: LIPUS alleviates gallbladder contractile dysfunction in acute cholecystitis by acting on ICCs through mechanisms involving the promotion of ICC recovery and a reduction in inflammation.