Tania Marchbank1, George Elia, Raymond J Playford. 1. Centre for Gastroenterology, Institute of Cell and Molecular Science, Barts and The London School of Medicine, Queen Mary University of London, UK.
Abstract
OBJECTIVES: 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). CONCLUSION: This natural bioactive product reduced apoptosis and the gut damaging effects of indomethacin.
OBJECTIVES: 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). CONCLUSION: This natural bioactive product reduced apoptosis and the gut damaging effects of indomethacin.