IB-MECA, an adenosine A3 receptor agonist, does not influence survival of lethally γ-irradiated mice

Title:

IB-MECA, an adenosine A3 receptor agonist, does not influence survival of lethally γ-irradiated mice

Creator:

Michal Hofer, Pospíšil, M., Dušek, L., Zuzana Hoferová, and Komůrková, D.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:a6a29dc5-df67-4e64-ad32-338665fb8374
uuid:a6a29dc5-df67-4e64-ad32-338665fb8374

Subject:

Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, mouse, IB-MECA, denosine A3 receptor agonist, lethal γ-irradiation, survival, 14, and 612

Type:

article, články, model:article, and TEXT

Description:

In our previous studies, IB-MECA, an adenosine A3 receptor agonist, was found to stimulate proliferation of hematopoietic progenitor and precursor cells in mice. This property of IB-MECA was considered to be responsible for its ability to support regeneration of suppressed hematopoiesis after irradiation with sublethal doses of γ-rays when the drug was given in a postirradiation treatment regimen. This study was aimed at assessing the ability of IB-MECA to influence a 30-day survival of lethally irradiated mice. In a series of experiments, IB-MECA was administered following various lethal radiation doses in various numbers of drug doses and various administration routes. Though in some of these experiments a moderate increase in 30-day survival was observed in IB-MECA-treated mice, the differences in comparison with the controls were not significantly different. It can be inferred from these results and those of previous studies assessing the effects of IB-MECA after sublethal radiation doses that IB-MECA can probably influence only a substantially preserved hematopoiesis like that remaining after sublethal irradiation. Future studies should be aimed at evaluation of the abilities of IB-MECA to influence post-irradiation survival when administered as a part of combined treatment regimens., M. Hofer, ... [et al.]., and Obsahuje seznam literatury

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2012 Volume:61 | Number:6

Harvested from:

CDK

Metadata only:

false