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Although the mechanism of stress-induced gastric ulcer has not been defined yet, it is clear that gastric ulcer is occurred by stress. Moreover, the gastric ulcerogenic action of corticosteroids that increase in blood during stress is controversial. To elucidate the involvement of corticosteroids in stress-induced gastric ulceration, we used adrenalectomized or macrophage-depleted animals. Rats were bilaterally-adrenalectomized and were given saline solution as a drinking water for 6 days. Separately, the animals for macrophage depletion were intraperitoneally administered with silica (SiO₂, 500 ㎎/㎏) for 6 days prior to challenge with water-immersion restraint stress (WIRS) for 4 hr. Adrenalectomy greatly reduced blood cortisol concentrations. Also, silica treatment lowered the number of macrophages to 48% of control and the differential count from 7.34% in normal animals to 2.48%, leading to a marked decrease in blood cortisol and corticosterone levels. WIRS significantly enhanced corticosteroid levels in normal and sham operated rats, and induced severe gastric ulcers. In contrast, adrenalectomy and silica treatment remarkably attenuated the stress-induced gastric ulceration, reducing the ulcer index to 30% and 10% of control level, respectively. Taken together, it is suggested that compensatory secretion of corticosteroids following macrophage activation may playa role in stress-induced gastric ulceration.

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UCI(KEPA) : I410-ECN-0101-2009-510-016363320