Intestinal protective effect of a commercial fish protein hydrolysate preparation.
OBJECTIVE
A partially hydrolysed, dried, product of pacific whiting fish is marketed as a health food supplement supporting 'intestinal health'. Scientific data supporting these claims are severely limited. We, therefore, examined if it influenced intestinal injury caused by the NSAID, indomethacin.


METHODS
Effects of fish hydrolysate on proliferation ([3H]-thymidine) and indomethacin-induced apoptosis (active caspase-3-immunostaining) utilised HT29 cells. In vivo studies used mice (n=8/group). 4/6 groups had fish hydrolysate (25 or 50 mg/ml) supplemented to their drinking water for 7 days. All mice received indomethacin (85 mg/kg subcutaneously) or placebo, 12 h before killing. Small intestinal injury was assessed using morphometry and morphology, proliferation (crypt BrdU labelling ) and apoptosis (active caspase-3 immunostaining).


RESULTS
Fish hydrolysate stimulated proliferation of HT29 cells. Apoptosis increased 3-fold following incubation with indomethacin but co-presence of fish hydrolysate truncated this effect by 40% (p<0.01). In mice, fish hydrolysate reduced the villus damaging effects of indomethacin by 60% (p<0.05). Indomethacin increased intestinal proliferation by 65%, irrespective of presence of hydrolysate. In contrast, intestinal caspase-3 activity increased by 83% in animals given indomethacin but this rise was truncated by 70% by co-presence of hydrolysate (p<0.01).


CONCLUSIONS
This natural bioactive product reduced apoptosis and the gut damaging effects of indomethacin.
Marchbank
Tania
T
Centre for Gastroenterology, Institute of Cell and Molecular Science, Barts and The London School of Medicine, Queen Mary University of London, UK.
Elia
George
G
Playford
Raymond J
RJ