Source comparison
BPC-157 for Constipation Research: Model Comparison
L-NAME-induced constipation (rat) NO pathway restoration 10 mcg/kg IP Fecal output, transit time Normal transit restored in 48–72h vs persistent dysfunction in controls Demonstrates NO-dependent mechanism. Strongest mechanistic evidence for motility restoratio
This comparison does not assign a generated winner or score.
- L-NAME-induced constipation (rat)
- NO pathway restoration
- 10 mcg/kg IP
- Fecal output, transit time
- Normal transit restored in 48–72h vs persistent dysfunction in controls
- Demonstrates NO-dependent mechanism. Strongest mechanistic evidence for motility restoration
- Atropine-induced hypomotility (rat)
- Compensation for cholinergic blockade
- Gastric emptying rate
- Partial reversal (40% improvement vs control)
- Suggests alternative pathway activation when primary cholinergic signaling blocked
- TNBS colitis (rat)
- Inflammation reduction, mucosal repair
- 10 mcg/kg IP daily × 14 days
- Colonic transit time, inflammation score
- 60% reduction in inflammation; transit time normalized
- Indicates motility improvement secondary to anti-inflammatory effect
- NSAID-induced enteropathy (rat)
- Mucosal protection, enteric neuron preservation
- Lesion count, nNOS neuron density
- 70% reduction in mucosal lesions; preserved nNOS neurons
- Shows neuroprotective effect relevant to drug-induced constipation
- Ischemia-reperfusion injury (rat)
- Angiogenesis, tissue perfusion
- 10 mcg/kg IP post-injury
- Blood flow restoration, motility recovery
- Accelerated vascular repair; motility recovered 5 days earlier than controls
- Suggests potential in vascular-origin motility disorders