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AIM:To investigate Tie-2 expression during the repair ofacetic acid-induced gastric ulcers in rats treated withrecombinant human IL-11(rhIL-11)and in untreated controlanimals.METHODS:Gastric ulcers were induced in male Wistar ratsby applying acetic acid to the fundus of the stomach.RhIL-11(100 μg/kg twice daily,subcutaneously)was administeredfrom two days before ulcer induction and continued for fivedays after the induction.Control rats received bovine serumalbumin.Gastric specimens were collected at 3 and 5 daysafter the induction of ulcer for immunohistochemicalobservation,Western blotting,and reverse transcriptionpolymerase chain reaction(RT-PCR).RESULTS:Immunohistochemical and Western blot analysisdemonstrated that Tie-2 expression was enhanced in therhIL-11-treated rats compared with the control animals atboth intervals.CONCLUSION:These findings suggested that IL-11 couldaccelerate ulcer healing,in part,by up-regulating Tie-2expression and promoting angiogenesis.
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 controlanimals. METHODS: Gastric ulcers were induced in male Wistar rats by applying acetic acid to the fundus of the stomach. RhIL-11 (100 μg / kg twice daily, subcutaneously) was administered from two days before ulcer induction and continued for five days after the induction. Control rats received bovine serumalbumin. 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 therhIL-11-treated rats compared with the control animals atboth intervals. CONCLUSION: These findings suggest that IL-11 couldaccelerate ulcer healing, in part, by up-regulating Tie-2 expression and promoting angiogenesis.