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由八肽胆囊收缩素、蛙皮素及其新型类似物诱导的小鼠过度刺激型胰腺炎:分子结构对效力的影响

Hyperstimulation pancreatitis in mice induced by cholecystokinin octapeptide, caerulein, and novel analogues: effect of molecular structure on potency.

作者信息

Shorrock K, Austen B M, Hermon-Taylor J

机构信息

Department of Surgery, St. Georges Hospital Medical School, London, England.

出版信息

Pancreas. 1991 Jul;6(4):404-6. doi: 10.1097/00006676-199107000-00005.

DOI:10.1097/00006676-199107000-00005
PMID:1715084
Abstract

Acute pancreatic oedema with hyperamylasaemia was induced in mice by subcutaneous administration of cholecystokinin octapeptide (CCK8). Comparison with effect of caerulein showed that cholecystokinin is less potent in vivo. To investigate the observed difference in response, threonine3 CCK8 and methionine5 caerulein were synthesised and evaluated. Comparison of these peptides suggests that difference in bioactivity is related to possession of extra N-terminal residues rather than substitution of threonine for methionine.

摘要

通过皮下注射八肽胆囊收缩素(CCK8)在小鼠中诱导出急性胰腺水肿伴高淀粉酶血症。与蛙皮素的作用比较表明,胆囊收缩素在体内的效力较低。为了研究观察到的反应差异,合成并评估了苏氨酸3 CCK8和蛋氨酸5蛙皮素。这些肽的比较表明,生物活性的差异与额外N端残基的存在有关,而不是苏氨酸取代蛋氨酸。

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1
Hyperstimulation pancreatitis in mice induced by cholecystokinin octapeptide, caerulein, and novel analogues: effect of molecular structure on potency.由八肽胆囊收缩素、蛙皮素及其新型类似物诱导的小鼠过度刺激型胰腺炎:分子结构对效力的影响
Pancreas. 1991 Jul;6(4):404-6. doi: 10.1097/00006676-199107000-00005.
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Impairment of intracellular calcium homoeostasis in the exocrine pancreas after caerulein-induced acute pancreatitis in the rat.大鼠蛙皮素诱导的急性胰腺炎后外分泌胰腺细胞内钙稳态的损伤
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Caerulein and cholecystokinin reverse experimental hemorrhagic shock.蛙皮素和胆囊收缩素可逆转实验性失血性休克。
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Bioactivity of cholecystokinin analogues: CCK-8 is not more potent than CCK-33.胆囊收缩素类似物的生物活性:八肽胆囊收缩素(CCK-8)的效力并不比三十三肽胆囊收缩素(CCK-33)更强。
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Experimental pancreatitis is mediated by low-affinity cholecystokinin receptors that inhibit digestive enzyme secretion.实验性胰腺炎是由抑制消化酶分泌的低亲和力胆囊收缩素受体介导的。
Proc Natl Acad Sci U S A. 1989 Nov;86(22):8968-71. doi: 10.1073/pnas.86.22.8968.

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