EFFECTS OF CHILLI AND CAPSAICIN ON THE GASTROINTESTINAL TRACT OF THE RAT

Abstract

Although both chilli and capsaicin retarded gastric empyting, there is no major effect on gasstric-small intestinal transit nor total gut transit in the rat. Chilli ingestion had no consistent effect on gastrotestinal mucosal proliferation nor an azoxymethane-induced colonic carcinogenesis.

We have shown both acute and chronic intragastric administration of chilli powder to have the same gastroprotective effecct as capsaicin on ethanol-induced gastric musosal injury. Chilli probably exerted its gastroprotective via its capsaicin content, since the protective effect was lost following sensory ablation.

Capsaicin had a limited effect on the healing of gastric mucosal injury following ethanol-induced damage as well as water immersion-immobilisation stress induced gastric mucosal injury. It had no prophylactic effect against water immersion-immobilisation stress-induced gastric mucosal injury.

Capsaicin promoted the healing of acetic acid-induced chronic gastric ulcer. This effect was probably mediated by its effect on gastric hyperaemia. Concomitant use of cimetidine, an ulcer healing agent which depressed gastric mucosal blood flow, reduced the ulcer healing effect of capsaicin. Capsaicin is therefore potentially useful as an ulcer healing agent in human peptic ulcer disease.

The gastroprotective effect of epidermal growth factor was lost following capsaicin desensitisation. Epidermal growth factor had no gastric hyperaemic effect in rats which have been subjected to sensory ablation, in contrast to rates with intact innervation. Concurrent administration of a calcitonin gene-related peptide antagonist, hCGRP8-37, abolished the gastric hyperaemic effect of both capsaicin and epidermal growth factor. This suggests that epidermal growth factor exerted its gastroprotective effect via capsaicin sensitive afferent neurones leading to release of calcitonin gene-related peptide with resultant gastric hyperaemia.