1994PubMedRequires access

[Medicinal activation and inhibition of function of glucocorticoid receptors as the basis for regulation of the glucocorticoid effect].

Golikov Pp

Open publisher page 1 citations

Abstract

On the basis of Scatchard and Lineweaver-Burk analysis, it was demonstrated that a series of drugs either activated or inhibited the function of types II and III glucocorticoid receptors. Analgine (0.04-10.0 mM) and sodium salicylate (12.5-50.0 mM) suppress the type II glucocorticoid receptor function of rat liver cytosol. Maradol (5.0 mM) increases the type II glucocorticoid receptors density but decreases the measurable constant for the [3H]acetonide triamsinolone interaction with type II glucocorticoid receptors. Analgine (1.25-10.0 mM) and sodium salicylate (0.62-10.0 mM) increase the type III glucocorticoid receptor function of rat liver cytosol. Maradol (0.25-1.0 mM) suppresses the type III glucocorticoid receptor function. The mechanism of regulation of the glucocorticoid effect by nonsteroid drugs influencing upon the function of types II and III glucocorticoid receptors is discussed.

About this research paper

What this paper is about

On the basis of Scatchard and Lineweaver-Burk analysis, it was demonstrated that a series of drugs either activated or inhibited the function of types II and III glucocorticoid receptors. Analgine (0.04-10.0 mM) and sodium salicylate (12.5-50.0 mM) suppress the type II glucocorticoid receptor function of rat liver cytosol. Maradol (5.0 mM) increases the type II glucocorticoid receptors density but decreases the measurable constant for the [3H]acetonide triamsinolone interaction with type II glucocorticoid receptors. Analgine (1.25-10.0 mM) and sodium salicylate (0.62-10.0 mM) increase the type III glucocorticoid receptor function of rat liver cytosol. Maradol (0.25-1.0 mM) suppresses the type III glucocorticoid receptor function. The mechanism of regulation of the glucocorticoid effect by nonsteroid drugs influencing upon the function of types II and III glucocorticoid receptors is discussed.

Why it matters

OpenAlex reports 1 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

On the basis of Scatchard and Lineweaver-Burk analysis, it was demonstrated that a series of drugs either activated or inhibited the function of types II and III glucocorticoid receptors. Analgine (0.04-10.0 mM) and sodium salicylate (12.5-50.0 mM) suppress the type II glucocorticoid receptor function of rat liver cytosol. Maradol (5.0 mM) increases the type II glucocorticoid receptors density but decreases the measurable constant for the [3H]acetonide triamsinolone interaction with type II glucocorticoid receptors. Analgine (1.25-10.0 mM) and sodium salicylate (0.62-10.0 mM) increase the type III glucocorticoid receptor function of rat liver cytosol. Maradol (0.25-1.0 mM) suppresses the type III glucocorticoid receptor function. The mechanism of regulation of the glucocorticoid effect by nonsteroid drugs influencing upon the function of types II and III glucocorticoid receptors is discussed.

Key concepts: Glucocorticoid receptor, Glucocorticoid, Receptor, Sodium salicylate, Endocrinology, Internal medicine, Cytosol, Chemistry

Related papers

Back to paper searchBrowse research topicsOriginal source
[Medicinal activation and inhibition of function of glucocorticoid receptors as the basis for regulation of the glucocorticoid effect]. — Research Paper | ScholarLens