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[前列腺素D2——生理性睡眠的内源性调节因子,抑制促肾上腺皮质激素释放因子诱导的大鼠垂体前叶细胞促肾上腺皮质激素分泌]

[Prostaglandin D2-endogenous regulator of physiological sleep-inhibited CRF-induced ACTH secretion from rat anterior pituitary cells].

作者信息

Kudo M, Kudo T, Matsuki A

机构信息

Department of Anesthesiology, University of Hirosaki School of Medicine.

出版信息

Nihon Naibunpi Gakkai Zasshi. 1990 Nov 20;66(11):1158-63. doi: 10.1507/endocrine1927.66.11_1158.

Abstract

Delta sleep-inducing peptide (DSIP) is described as being an endogenous sleep factor. This DSIP inhibits ACTH release induced by CRF from rat anterior pituitary tissue. Prostaglandin D2 (PGD2) is regarded as another endogenous sleep factor. However, little information has been accumulated concerning the involvement of PGD2 in the regulation of hormone secretion from the anterior pituitary. It was, therefore, interesting to observe the effect of PGD2 on ACTH release from rat anterior pituitary cells. Rat anterior pituitary cells were obtained by enzymatic digestion of the pituitary gland of male Wister rats. The cell pellet was suspended in Hank's balanced salt solution containing 0.1% BSA and distributed in a 800 microliter aliquot to 12 x 75mm glass tubes. The samples were preincubated for 90 min. in a 37 degrees C waterbath under 5% CO2/95% O2. After preincubation, aliquots of various concentrations of CRF, PGD2 and PGE2 were added in a 100 microliter volume and incubated for 4 hr. ACTH in the incubation medium was determined by radioimmunoassay. 0.01-1.0nM CRF significantly increased the ACTH release from rat anterior pituitary cells in a dose dependent manner. Each concentration of 0.1, 1, 2nM PGD2 or PGE2 had no effect on basal ACTH levels. 2nM PGD2 showed a significant inhibition of the CRF-induced ACTH secretion from rat anterior pituitary cells. Similarly, 2nM PGE2 significantly inhibited the CRF-induced ACTH release from rat anterior pituitary cells. The magnitude of the inhibitory effect of PGE2 was slightly higher than that of PGD2. From these results, we concluded that PGD2 inhibited CRF-induced ACTH secretion at the level of pituitary gland.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

δ-睡眠诱导肽(DSIP)被描述为一种内源性睡眠因子。这种DSIP可抑制促肾上腺皮质激素释放因子(CRF)诱导的大鼠垂体前叶组织中促肾上腺皮质激素(ACTH)的释放。前列腺素D2(PGD2)被视为另一种内源性睡眠因子。然而,关于PGD2参与垂体前叶激素分泌调节的信息积累较少。因此,观察PGD2对大鼠垂体前叶细胞ACTH释放的影响很有意思。通过酶消化雄性Wistar大鼠的垂体获得大鼠垂体前叶细胞。将细胞沉淀悬浮于含0.1%牛血清白蛋白的汉克平衡盐溶液中,并以800微升的等分试样分配到12×75毫米的玻璃管中。样品在37℃、5%二氧化碳/95%氧气的水浴中预孵育90分钟。预孵育后,加入不同浓度的CRF、PGD2和前列腺素E2(PGE2)的100微升等分试样,并孵育4小时。通过放射免疫分析法测定孵育培养基中的ACTH。0.01 - 1.0纳摩尔的CRF以剂量依赖性方式显著增加大鼠垂体前叶细胞中ACTH的释放。0.1、1、2纳摩尔的PGD2或PGE2各浓度对基础ACTH水平均无影响。2纳摩尔的PGD2显著抑制CRF诱导的大鼠垂体前叶细胞中ACTH的分泌。同样,2纳摩尔的PGE2显著抑制CRF诱导的大鼠垂体前叶细胞中ACTH的释放。PGE2的抑制作用程度略高于PGD2。从这些结果我们得出结论,PGD2在垂体水平抑制CRF诱导的ACTH分泌。(摘要截断于250字)

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