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Enhanced serum glucocorticoid levels mediate the reduction of serosal mast cell numbers in diabetic rats

机译:血清糖皮质激素水平升高介导糖尿病大鼠浆膜肥大细胞数量减少

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摘要

Rats turned diabetic by treatment with alloxan exhibit a significant reduction in serosal mast cell numbersin parallel with decreased insulin levels in the plasma. Our aim was to investigate the putative involvement of endogenous glucocorticoid hormone in this phenomenon. The findings indicated that rats treated with alloxan responded with an increase in levels of serum corticosterone concomitantly with decreased mast cell numbers in the pleural space. We found that either surgical bilateral adrenalectomy or pretreatment with the steroid antagonist RU 486 (20 mg/kg, i.p.) impaired the drop in pleural mast cell counts in alloxinated rats. Administration of insulin (15 U/kg) prevented the increase in corticosterone levels and restored pleural mast cell levels in diabetic animals. In addition, treatment of naive rats with corticosterone (0.5 mg/kg, s.c.) or dexamethasone (0.1 mg/kg, s.c.),for 3 consecutive days, led to a reduction in the number of mast cells recovered from the pleural cavity as noted in diabetic animals. In contrast, insulin reduced serum corticosterone levels and induced a significant elevation in pleural mast cell numbers in naive rats. We conclude that there is a causative relationship between increased levels of glucocorticoids and down-regulation of mast cell numbers associated with the diabetic state, both phenomena clearly sensitive to insulin. (C) 2001 Elsevier Science Inc. All rights reserved. [References: 23]
机译:用四氧嘧啶治疗变成糖尿病的大鼠浆膜肥大细胞数量显着减少,同时血浆中胰岛素水平降低。我们的目的是调查内源性糖皮质激素在这种现象中的推测参与。研究结果表明,用四氧嘧啶治疗的大鼠,其血清皮质酮水平升高,而胸膜腔内的肥大细胞数量减少,对此有反应。我们发现,无论是手术方式的双侧肾上腺切除术还是类固醇拮抗剂RU 486(20 mg / kg,i.p.)预处理均会损害同种异体氧化大鼠胸膜肥大细胞计数的下降。在糖尿病动物中,给予胰岛素(15 U / kg)可防止皮质酮水平升高并恢复胸膜肥大细胞水平。此外,连续3天用皮质酮(0.5 mg / kg,sc)或地塞米松(0.1 mg / kg,sc)治疗幼稚大鼠,导致从胸膜腔中回收的肥大细胞数量减少在糖尿病动物中。相反,在幼稚大鼠中,胰岛素降低了血清皮质酮水平,并导致胸膜肥大细胞数量显着升高。我们得出的结论是,糖皮质激素水平的升高与与糖尿病状态相关的肥大细胞数量的下调之间存在因果关系,这两种现象均明显对胰岛素敏感。 (C)2001 Elsevier Science Inc.保留所有权利。 [参考:23]

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