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通过生物测定法测定口服胰蛋白酶抑制剂后大鼠肠道胆囊收缩素的释放。

The release of rat intestinal cholecystokinin after oral trypsin inhibitor measured by bio-assay.

作者信息

Brand S J, Morgan R G

出版信息

J Physiol. 1981;319:325-43. doi: 10.1113/jphysiol.1981.sp013911.

DOI:10.1113/jphysiol.1981.sp013911
PMID:7320918
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1243841/
Abstract

The distribution, molecular form and release of cholecystokinin (CCK)-like activity in extracts of rat small intestine was studied with an in vitro gall-bladder bio-assay. In contrast to the reported heterogeneity of CCK-like immunoreactivity in the intestine, only a single molecular form of CCK-like activity was detected using the bio-assay. 2. The CCK-like activity eluted from Sephadex G50 with a Kav of 0.69, after the triacontriapeptide of cholecystokinin (CCK33) and before cholecystokinin octapeptide 2500, may represent the 22 amino acid peptide of CCK (CCK22). The bio-assay peak of CCK-like activity had pancreozymin activity and CCK/gastrin C terminal immunoreactivity. The CCK-like activity weas readily extracted from the small intestine at neutral pH, but subsequent treatment with cold 0.5 M-acetic acid extracted further CCK-like activity of the same molecular form as that recovered under neutral conditions. 3. The bio-assay detected no CCK-like activity, nor was pancreozymin-like activity found in fractions corresponding to CCK33 or CCK8 after Sephadex G50 chromatography of rat intestinal extracts. 4. Oral trypsin inhibitor was a potent stimulus for the release of CCK-like activity from the upper small intestine of the rat. After oral trypsin inhibitor release, CCK-like activity was rapidly resynthesized.

摘要

采用体外胆囊生物测定法,研究了大鼠小肠提取物中胆囊收缩素(CCK)样活性的分布、分子形式及释放情况。与报道的小肠中CCK样免疫反应性的异质性不同,使用该生物测定法仅检测到单一分子形式的CCK样活性。2. 从Sephadex G50洗脱的CCK样活性,其洗脱体积(Kav)为0.69,在胆囊收缩素三十肽(CCK33)之后、胆囊收缩素八肽2500之前,可能代表CCK的22氨基酸肽(CCK22)。CCK样活性的生物测定峰具有促胰酶素活性和CCK/胃泌素C末端免疫反应性。CCK样活性在中性pH值下很容易从小肠中提取出来,但随后用冷的0.5M乙酸处理会进一步提取出与在中性条件下回收的相同分子形式的CCK样活性。3. 生物测定未检测到CCK样活性,大鼠肠提取物经Sephadex G50层析后,在对应于CCK33或CCK8的组分中也未发现促胰酶素样活性。4. 口服胰蛋白酶抑制剂是大鼠上段小肠释放CCK样活性的有效刺激物。口服胰蛋白酶抑制剂释放后,CCK样活性迅速重新合成。

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