AI Article Synopsis
- TGF-alpha plays a protective role against stomach mucosal injury caused by ethanol, but the exact mechanisms are not fully understood.
- Researchers conducted experiments on fasted rats to assess the contributions of sensory neurons, neuropeptides (CGRP and substance P), and prostaglandins to this gastroprotective effect.
- The study found that TGF-alpha significantly reduced gastric lesions and relied on the activation of sensory neurons and release of CGRP, while neither substance P nor prostaglandins were necessary for this protection.
Article Abstract
The mechanisms by which transforming growth factor-a (TGP-alpha) protects the stomach against mucosal injury are incompletely understood. The aim of this study was to examine the roles of sensory neurons, sensory neuropeptides and prostaglandins in TGFalpha gastroprotection against ethanol. Fasted rats received TGF-alpha (50 microg/kg, intraperitoneally) prior to orogastric ethanol (75% v/v, 1 ml). Gastric injury was quantitated 30 min after ethanol. Involvement of sensory neurons and the sensory neuropeptides, calcitonin gene-related peptide (CGRP) and substance P (SP), were examined by capsaicin deafferentation and specific receptor antagonist infusion, respectively. Indomethacin (10 mg, intragastrically) was used to determine the role of prostaglandins in TGF-alpha-mediated gastroprotection. TGF-alpha significantly diminished ethanol-induced gastric lesion area to 5.7 +/- 0.8 mm2 vs 41.1 +/- 5.2 mm2 (p < 0.001). Sensory denervation and CGRP-receptor blockade abolished the TGF-alpha protective effect. In contrast, SP antagonist and indomethacin did not alter TGF-alpha gastroprotection. In conclusion, TGF-alpha-mediated gastroprotection involves sensory neuron activation and CGRP release and this protective effect did not involve substance P or prostaglandin generation.
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| http://dx.doi.org/10.1023/a:1021935728607 | DOI Listing |
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