capsazepine and Enteritis

capsazepine has been researched along with Enteritis* in 1 studies

Other Studies

1 other study(ies) available for capsazepine and Enteritis

Article	Year
The capsaicin VR1 receptor mediates substance P release in toxin A-induced enteritis in rats. Peptides, 2001, Volume: 22, Issue:9 The mechanism by which Clostridium difficile toxin A causes substance P (SP) release and subsequent inflammation in the rat ileum is unknown. Pretreatment with the vanilloid receptor subtype 1 (VR1) antagonist, capsazepine, before toxin A administration significantly inhibited toxin A-induced SP release and intestinal inflammation. Intraluminal administration of the VR1 agonist capsaicin caused intestinal inflammation similar to the effects of toxin A. Pretreatment with capsazepine before capsaicin administration also significantly inhibited capsaicin-induced intestinal inflammation. These results suggest that intraluminal toxin A causes SP release from primary sensory neurons via stimulation of VR1 receptors resulting in intestinal inflammation. Topics: Acute-Phase Reaction; Animals; Bacterial Toxins; Capsaicin; Clostridioides difficile; Dose-Response Relationship, Drug; Drug Interactions; Endocytosis; Enteritis; Enterotoxins; Ileum; Immunohistochemistry; Intestinal Secretions; Male; Neurogenic Inflammation; Neurons; Peroxidase; Rats; Receptors, Drug; Substance P; Time Factors	2001

Article

Year

The capsaicin VR1 receptor mediates substance P release in toxin A-induced enteritis in rats.

Peptides, 2001, Volume: 22, Issue:9

The mechanism by which Clostridium difficile toxin A causes substance P (SP) release and subsequent inflammation in the rat ileum is unknown. Pretreatment with the vanilloid receptor subtype 1 (VR1) antagonist, capsazepine, before toxin A administration significantly inhibited toxin A-induced SP release and intestinal inflammation. Intraluminal administration of the VR1 agonist capsaicin caused intestinal inflammation similar to the effects of toxin A. Pretreatment with capsazepine before capsaicin administration also significantly inhibited capsaicin-induced intestinal inflammation. These results suggest that intraluminal toxin A causes SP release from primary sensory neurons via stimulation of VR1 receptors resulting in intestinal inflammation.

Topics: Acute-Phase Reaction; Animals; Bacterial Toxins; Capsaicin; Clostridioides difficile; Dose-Response Relationship, Drug; Drug Interactions; Endocytosis; Enteritis; Enterotoxins; Ileum; Immunohistochemistry; Intestinal Secretions; Male; Neurogenic Inflammation; Neurons; Peroxidase; Rats; Receptors, Drug; Substance P; Time Factors

2001