The Experiment Of Curcumin On Experimental Necrotizing Enterocolitis

PartⅠIMPROVEMENT AND COMPARISON OF ANIMAL MODELS OF NEONATAL NECROTIZING ENTEROCOLITISObjective:To establish a new animal model of neonatal necrotizing enterocolitis(NEC) by cold exposure after hypoxic- reoxygenation treatment , formula feeding and LPS intragastric administration on the base of the modeling status ,and to compare the differences between them .Methods: According to different modeling methods, 0-day-postnatal S-D rats were divided into 6 groups randomly, each group including 8 rats. Group A was given cold exposure shortly after hypoxic-reoxygen treatment and received formula feeding. Group B was in the same condition expect extra LPS intragastric administration. Group C was given cold exposure after simple hypoxic- reoxygenation treatment . Group D received LPS intragastric administration. Group E was given formula feeding alone. Group F was set up as control group. All rats were weighed every day and sacrificed on the 4th day. Proximal intestines of ileocecal junction were harvested and were evaluated by HE staining for pathological scoring.Results: All the neonatal rats in model groups had physical inactivity, abdominal distention and a change in stool . On day 3, neonatal rats in group A,B,and E had weight loss, while group C,D,and F had weight gain. The terminal weight and weight change of every model group were different from that of Group F(P<0.05).By Kruskal-wallis analysis, weight changes of each group were:Group F> Group D> Group C > Group E > Group A > Group B. The pathological scores ( x-±s) for each gourp were group A :3.0±0.53, group B:3.63±0.52, group C:1.75±0.71,group D: 1.75±0.46,group E: 2.38±0.52 and group F 0.5±0.53 respectively .The score of group B had significant differences from those of other 5 groups(P<0.05). Cold exposure after hypoxic-reoxygenation, formula feeding and LPS intragastric administration were all risk factors for NEC.Our new method with combination of all these factors could produce the most serious intestine injury.Conclusions: By cold exposure after hypoxic-reoxygenation, formula feeding and LPS intragastric administration, we could produced animal models which had intestine injury similar to neonatal necrotizing enterocolitis. This new method could be used for the establishment of NEC animal modle extensively. PartⅡTHE EFFECT AND POSSIBLE MECHANISM OF CURCUMIN ON EXPERIMENTAL NECROTIZING ENTEROCOLITISObjective: To observe effects of curcumin on experimental necrotizing enterocolitis, and to investigate the potential pathogenetic mechanism.Methods: Twenty four 0-day-postnatal S-D rats were divided into 3 groups randomly, each group include 8 rats. GroupⅠwas given treatment as model group as described before, GroupⅡwas in the same condition expect extra curcumin intraperitoneally infused. GroupⅢwas set up as a control. All rats were weighed every day and sacrificed on the 4th day. Proximal intestines of ileocecal junction were harvested and were evaluated by HE staining for pathological scoring. The activity of intestines MDA,SOD and the expression of HO-1 in all rats was also detected respectively.Results: Compare to groupⅢ, rats in groupⅡhad better growing development and physical inactivity than groupⅠ. The gross characteristics were greatly improved in groupⅡcompared to groupⅠ. The pathological score of groupⅠandⅡhad significant differences against the groupⅢ(P<0.05) , while difference betweenⅠandⅡgroups is statistically significant (P<0.05).The contents of intestine MDA were higher than groupⅢfor the other two groups, but groupⅡwere lower than groupⅠ. We have found that there was a great decrease of the SOD activity of groupⅠcompared to groupⅢ(P<0.05), while groupⅡwas higher than groupⅢ, but the difference fell short of statistical significance. The expression of HO-1 was significant increased in groupⅠand groupⅡ, and difference between the two groups is statistically significant (P<0.05).Conclusions: Curcumin has positive effection in treating experimental necrotizing enterocolitis . Curcumin reduces intestinal oxidative damage through rising the expression of HO-1, decreasing the content of intestine MDA, and enhancing the activity of SOD.