News Release

Wuda granule improves the gastrointestinal motility via gut-brain axis in beagle dogs

Peer-Reviewed Publication

FAR Publishing Limited

Figure 1A. Gastrointestinal MMC curves chart in beagle dogs. Figure 1B. Gastrointestinal motility curve chart in beagle dogs before and after lateral ventricular injection of WDG in awake and fasted state. Figure 1C. Gastrointestinal motility curve chart

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Figure 1A:In the awaken and fasted state, typical MMC contractile movements were seen in the gastric body, sinus, duodenum and jejunum in beagle dogs, while the colon was dominated by intermittent clustered contractions and resting periods.

 Figure 1B:In awake and fasted state, the gastric body, In awake and fasted state, after the resting phase of MMC phase I, injections of WDG at 5 mg in the lateral ventricles were observed to show more intense contractions of longer duration than in the anesthetized state at the same dose.

Figure 1C:Before and after saline administration, the gastric body, antrum, duodenum, jejunum, and colon of the beagle dog showed no obvious contractions, displaying a pattern characteristic of the MMC phase I.

Figure 1D:Animals received an intracerebroventricular injection of vehicle (20 µL normal salin) or WDG at 1.25, 2.5, or 5 mg (20 µL, n = 12 per group) in random. MMC activity was continuously recorded for 2 h post-injection. Compared to control group, **** P<0.0001, ***P<0.001, **P<0.01. n=12.

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Credit: Zhi Jiang, Xing Li ,Qicheng Chen, Zhiqiang Chen, Lixing Cao, Hailin Tang

This study investigated the mechanism of Wuda granule (WDG) on gastrointestinal (GI) motility in beagle dogs. Stress sensors implanted in the stomach, duodenum, jejunum, and colon recorded contractile activity. Lateral ventricular administration of WDG (5mg) significantly enhanced contractile motility in all recorded GI regions in awake dogs; this effect was attenuated under intravenous anesthesia. The prokinetic effect of central WDG was completely blocked by intravenous atropine infusion [50 μg/(kg·h)]. Bilateral cervical vagotomy prolonged the migrating motor complex cycle, weakened gastric phase III contractions, and abolished the WDG-induced enhancement specifically in the stomach. However, WDG still enhanced motility in the duodenum, jejunum, and colon post-vagotomy. Transmission electron microscopy confirmed no intestinal structural changes induced by WDG. WDG enhances GI contractility centrally, primarily via activation of vagal cholinergic pathways for the stomach, while exerting effects on the lower GI tract through additional, non-vagal mechanisms.


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