Abstract:Objective The intestinal trefoil factor (ITF) is closely related with gastrointestinal epithelial cells injury repair. Studying the effects of ITF on necrotizing enterocolitis (NEC) would be helpful to the treatment of NEC. This research investigated the effect of ITF on intestinal histopathological changes, expression of cyclooxygenase-2 (COX-2 ) and the production of prostaglandin E 2 (PGE 2 )and thromboxane B 2 (TXB 2) in neonatal rats with NEC.Methods Forty one-day-old Wistar rats were randomly divided into 5 groups: Groups A, B, C, D and E (n=8 each). Group A served as the normal control group. Rats in Groups B, C, D and D were made into NEC models by hypoxia and re-oxygenation for 3 consecutive days. Groups D and E were treated with 0.5 mL ITF ( 0.5 mg) intraperitoneal injection or 0.2 mL ITF ( 0.2 mg) subcutaneous injection once respectively after damage, while Groups B and E were injected with normal saline intraperitoneally or subcutaneously respectively. On the 4th day all the subjects were sacrificed and intestinal tissues were obtained to examine the histological changes, COX-2 expression, and PGE 2 and TXB 2 productions. Results Intestinal histopathology of rats in Group A was normal, and the pathologic scores were 0. As compared with the corresponding NEC group(Groups B and C), histopathological injuries of NEC were remarkably relieved after ITF treatment (Groups D and E)(P < 0.01). The pathologic scores of rats in Groups B and C were 1- 4, while those of Groups D and E were 0-2. PGE 2 and TXB 2 contents significantly increased in Groups B and C, while dramatically decreased after ITF treatment (in Groups D and E). No significant differences were observed for the PGE 2 and TXB 2 contents between Groups D, E and A. Immunohistochemistry staining indicated positive expression of COX-2 in Groups B and C, which were significantly higher than Groups A, D and E (P < 0.05). Mild positive expression of COX-2 was observed in Groups D and E, which was stronger than Group A. Conclusions ITF can decrease the productions of PGE 2 and TXB 2 by suppressing the expression of COX-2, which may be underlying protective mechanisms of ITF on NEC.
