AIM: To investigate Tie-2 expression during the repair of acetic acid-induced gastric ulcers in rats treated with recombinant human IL-11 (rhIL-11) and in untreated control animals.METHODS: Gastric ulcers were induced...AIM: To investigate Tie-2 expression during the repair of acetic acid-induced gastric ulcers in rats treated with recombinant human IL-11 (rhIL-11) and in untreated control animals.METHODS: Gastric ulcers were induced in male Wistar rats by applying acetic acid to the fundus of the stomach. RhIL-11 (100μg/kg twice daily, subcutaneously) was administered from two days before ulcer induction and continued for five days after the induction. Control rats received bovine serum albumin. Gastric specimens were collected at 3 and 5 days after the induction of ulcer for immunohistochemical observation, Western blotting, and reverse transcription polymerase chain reaction (RT-PCR).RESULTS: Immunohistochemical and Western blot analysis demonstrated that Tie-2 expression was enhanced in the rhIL-11-treated rats compared with the control animals at both intervals.CONCLUSION: These findings suggested that IL-11 could accelerate ulcer healing, in part, by up-regulating Tie-2 expression and promoting angiogenesis.展开更多
文摘AIM: To investigate Tie-2 expression during the repair of acetic acid-induced gastric ulcers in rats treated with recombinant human IL-11 (rhIL-11) and in untreated control animals.METHODS: Gastric ulcers were induced in male Wistar rats by applying acetic acid to the fundus of the stomach. RhIL-11 (100μg/kg twice daily, subcutaneously) was administered from two days before ulcer induction and continued for five days after the induction. Control rats received bovine serum albumin. Gastric specimens were collected at 3 and 5 days after the induction of ulcer for immunohistochemical observation, Western blotting, and reverse transcription polymerase chain reaction (RT-PCR).RESULTS: Immunohistochemical and Western blot analysis demonstrated that Tie-2 expression was enhanced in the rhIL-11-treated rats compared with the control animals at both intervals.CONCLUSION: These findings suggested that IL-11 could accelerate ulcer healing, in part, by up-regulating Tie-2 expression and promoting angiogenesis.
