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Adding to the disease burden, poor survival is attributed to delayed diagnosis, malnutrition, bacterial colonization, and related complications (95)
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Summary BPC-157’s GI motility research biology operates through multiple intersecting mechanisms: nNOS-NO pathway modulation (GE and transit restoration in L-NAME and STZ gastroparesis models), dopaminergic pathway interactions (haloperidol and apomorphine dysmotility reversal), serotonin/SSRI-GI side effect attenuation (SERT, EC cell, and serotonin syndrome contexts), ICC preservation in diabetic models, macrophage-neuroinflammation suppression in post-operative ileus, and ENS neuroprotection assessed by LMMP wholemount histology
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