The gastric antisecretory activity of 3-methoxy-5,7,3′4′-tetrahydroxyflavan (ME)—a specific histidine decarboxylase inhibitor in rats

1984 ◽  
Vol 15 (3-4) ◽  
pp. 143-145 ◽  
Author(s):  
N. S. Parmar ◽  
G. Hennings
Keyword(s):  
Histidine Decarboxylase ◽  
Decarboxylase Inhibitor ◽  
Antisecretory Activity

Treatment of two mastocytosis patients with a histidine decarboxylase inhibitor

1985 ◽  
Vol 16 (3-4) ◽  
pp. 244-248 ◽  
Author(s):  
G. Granerus ◽  
J. H. Olafsson ◽  
G. Roupe
Keyword(s):  
Histidine Decarboxylase ◽  
Decarboxylase Inhibitor

Pinocembrin, a novel histidine decarboxylase inhibitor with anti-allergic potential in in vitro

2017 ◽  
Vol 814 ◽  
pp. 178-186 ◽  
Author(s):  
Hamza Hanieh ◽  
Villianur Ibrahim Hairul Islam ◽  
Subramanian Saravanan ◽  
Muthiah Chellappandian ◽  
Kessavane Ragul ◽  
...  
Keyword(s):  
Histidine Decarboxylase ◽  
Decarboxylase Inhibitor

The effects of drugs on worm expulsion in theNippostrongylus brasiliensisinfected rat: a discussion of the interpretation of drug action

Parasitology ◽  
1972 ◽  
Vol 64 (2) ◽  
pp. 217-227 ◽  
Author(s):  
R. Keller ◽  
Bridget M. Ogilvie
Keyword(s):  
Technical Assistance ◽  
Statistical Evaluation ◽  
Histidine Decarboxylase ◽  
Drug Action ◽  
Decarboxylase Inhibitor ◽  
Release Mechanisms ◽  
Worm Expulsion

In rats treated with compound 48/80 or histamine, worm expulsion was inhibited. Treatment with a histidine decarboxylase inhibitor accelerated worm expulsion. Treatment with compound 48/80 elevates histamine and histidine decarboxylase levels and reduces circulating reagin titres. These results show that histamine is not responsible for worm expulsion.Compounds such as isoprenaline and theophylline which increase cellular levels of cyclic 3′,5-AMP, prevented worm expulsion.It is concluded that the evidence that amines are involved in worm expulsion needs reassessing and that cellular release mechanisms in general may be affected by drugs thought to act solely on amine release. In particular, the release of effector substances from sensitized lymphocytes on contact with antigen may be affected by these treatments.The skilful technical assistance of Miss R. Keist and Miss I. Beeger is gratefully acknowledged. We thank Mr H. Berchtold, Biostatistisches Zentrum der Universität Zürich, for the statistical evaluation of the data.

The influence of α-fluoromethylhistidine on the regional brain histamine and plasma corticosterone levels in aging

1987 ◽  
Vol 65 (10) ◽  
pp. 2154-2157 ◽  
Author(s):  
I. Mazurkiewicz-Kwilecki ◽  
Simon Nsonwah
Keyword(s):  
Histidine Decarboxylase ◽  
Brain Regions ◽  
Plasma Corticosterone ◽  
Decarboxylase Inhibitor ◽  
Brain Histamine ◽  
Regional Brain ◽  
Histamine Synthesis ◽  
Hypothalamic Histamine ◽  
Old Rats

α-Fluoromethylhistidine, a histidine decarboxylase inhibitor, induced a significant depletion in the hypothalamic, midbrain, and cortical brain histamine amounts in 12- and 3-month-old rats. In all three brain regions the most evident depletion occurred 2 h after treatment. In both groups of rats midbrain histamine levels returned to control values 6 h after treatment; however, hypothalamic histamine depletion was still significant and more evident in the old than in the young animals. Cortical brain histamine also remained significantly depleted in old rats, but returned to control values in young animals 6 h after α-fluoromethylhistidine treatment. These results suggest that old rats show a slower rate of new histamine synthesis in the cortex and hypothalamus. Regional brain histamine depletion was associated with a very significant decrease in plasma corticosterone levels, which indicates that brain histamine–corticosterone interactions do occur.

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