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[亮氨酸5] -脑啡肽在三种离体标本中的失活:氨肽酶、内肽酶-24.11和肽基二肽酶A的相对重要性。

Inactivation of [Leu5]-enkephalin in three isolated preparations: relative importance of aminopeptidase, endopeptidase-24.11 and peptidyl dipeptidase A.

作者信息

Oka T, Aoki K, Kajiwara M, Ishii K, Kuno Y, Hiranuma T, Matsumiya T

机构信息

Department of Pharmacology, School of Medicine, Tokai University, Isehara, Japan.

出版信息

NIDA Res Monogr. 1986;75:259-62.

PMID:2828976
Abstract

Enkephalin had been shown to be almost exclusively hydrolyzed by three peptidases in the previous studies. In the present investigation, the relative importance of three enzymes in the inactivation of [Leu5]-enkephalin was examined in three isolated preparations. Results showed that amastatin-sensitive aminopeptidase played the greatest role in both guinea-pig ileum and rat vas deferens while it played the similar role to either phosphoramdidon-sensitive endopeptidase-24.11 or captopril-sensitive peptidyl dipeptidase A in mouse vas deferens.

摘要

在先前的研究中已表明脑啡肽几乎完全由三种肽酶水解。在本研究中,在三种离体标本中检测了这三种酶在[亮氨酸5] - 脑啡肽失活中的相对重要性。结果表明,氨肽酶抑制剂敏感的氨肽酶在豚鼠回肠和大鼠输精管中起最大作用,而在小鼠输精管中它与磷酰胺脒敏感的内肽酶-24.11或卡托普利敏感的肽基二肽酶A起相似作用。

相似文献

1
Inactivation of [Leu5]-enkephalin in three isolated preparations: relative importance of aminopeptidase, endopeptidase-24.11 and peptidyl dipeptidase A.[亮氨酸5] -脑啡肽在三种离体标本中的失活:氨肽酶、内肽酶-24.11和肽基二肽酶A的相对重要性。
NIDA Res Monogr. 1986;75:259-62.
2
The inactivation of [Met5]-enkephalin by bestatin-sensitive aminopeptidase, captopril-sensitive peptidyl dipeptidase A and thiorphan-sensitive endopeptidase-24.11 in mouse vas deferens.小鼠输精管中由贝司他汀敏感的氨肽酶、卡托普利敏感的肽基二肽酶A和硫氧还蛋白敏感的内肽酶-24.11对[Met5]-脑啡肽的失活作用。
Jpn J Pharmacol. 1986 Feb;40(2):297-302. doi: 10.1254/jjp.40.297.
3
Estimation of relative importance of three enzymes in the inactivation of [Met5]-enkephalin and [Met5]-enkephalin-Arg6 in three isolated preparations by employing the inhibitor specific for each enzyme.
Jpn J Pharmacol. 1987 Jul;44(3):241-7. doi: 10.1254/jjp.44.241.
4
Protection against dynorphin-(1-8) hydrolysis in membrane preparations by the combination of amastatin, captopril and phosphoramidon.通过阿马astatin、卡托普利和磷酰胺脒组合对膜制剂中强啡肽-(1-8)水解的保护作用。
J Pharmacol Exp Ther. 1998 Aug;286(2):863-9.
5
Almost complete protection from [Met5]-enkephalin-Arg6-Gly7-Leu8 (Met-enk-RGL) hydrolysis in membrane preparations by the combination of amastatin, captopril and phosphoramidon.通过阿马astatin、卡托普利和磷酰胺脒的联合使用,在膜制剂中几乎能完全保护[Met5]-脑啡肽-Arg6-Gly7-Leu8(Met-脑啡肽-RGL)不被水解。
J Pharmacol Exp Ther. 1997 May;281(2):769-74.
6
The enhancing effects of amastatin, phosphoramidon and captopril on the potency of [Met5]-enkephalin in rat vas deferens.氨肽酶抑制剂、磷酰胺脒和卡托普利对[Met5]-脑啡肽在大鼠输精管中效力的增强作用。
Jpn J Pharmacol. 1986 Sep;42(1):43-9. doi: 10.1254/jjp.42.43.
7
Inactivation of dynorphin-(1-8) in isolated preparations by three peptidases.三种肽酶对分离制剂中强啡肽-(1-8)的失活作用。
Jpn J Pharmacol. 1988 Aug;47(4):417-23. doi: 10.1254/jjp.47.417.
8
The relative potency of enkephalins and beta-endorphin in guinea-pig ileum, mouse vas deferens and rat vas deferens after the administration of peptidase inhibitors.给予肽酶抑制剂后,脑啡肽和β-内啡肽在豚鼠回肠、小鼠输精管和大鼠输精管中的相对效价。
Jpn J Pharmacol. 1986 Jul;41(3):273-81. doi: 10.1254/jjp.41.273.
9
[Enkephalin-inactivating enzymes].[脑啡肽失活酶]
Nihon Yakurigaku Zasshi. 1993 Apr;101(4):197-207. doi: 10.1254/fpj.101.4_197.
10
Effects of three peptidase inhibitors, amastatin, captopril and phosphoramidon, on the hydrolysis of [Met5]-enkephalin-Arg6-Phe7 and other opioid peptides.三种肽酶抑制剂,抑氨肽酶素、卡托普利和磷酰胺素,对[Met5]-脑啡肽-Arg6-Phe7及其他阿片肽水解的影响。
Naunyn Schmiedebergs Arch Pharmacol. 1998 Mar;357(3):276-82. doi: 10.1007/pl00005168.

引用本文的文献

1
Effect of three peptidase inhibitors on antinociceptive potential and toxicity with intracerebroventricular administration of dynorphin A (1-17) or (1-13) in the rat.三种肽酶抑制剂对大鼠侧脑室给予强啡肽 A(1-17)或(1-13)的镇痛潜力和毒性的影响。
J Anesth. 2015 Feb;29(1):65-77. doi: 10.1007/s00540-014-1860-4. Epub 2014 Jun 19.
2
Peptidases prevent mu-opioid receptor internalization in dorsal horn neurons by endogenously released opioids.肽酶可通过内源性释放的阿片类物质阻止背角神经元中的μ-阿片受体内化。
J Neurosci. 2003 Mar 1;23(5):1847-58. doi: 10.1523/JNEUROSCI.23-05-01847.2003.