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Zymosan-a Protects the Hematopoietic System from Radiation-Induced Damage by Targeting TLR2 Signaling Pathway.
Cell Physiol Biochem ; 43(2): 457-464, 2017.
Article en En | MEDLINE | ID: mdl-28922655
ABSTRACT
BACKGROUND/

AIMS:

The hematopoietic system is vulnerable to ionizing radiation and is often severely damaged by radiation. Molecules affecting radioresistance include Toll-like receptor 2. We investigated whether Zymosan-A, a novel TLR2 agonist, can protect the hematopoietic system from radiation-induced damage after total body irradiation.

METHODS:

Mice were exposed to total body radiation after treatment with Zymosan-A or normal saline, and their survival was recorded. Tissue damage was evaluated by hematoxylin-eosin staining. The number of nucleated cells in bone marrow was determined by flow cytometry. Cell viability and apoptosis assay were determined by CCK-8 assay and flow cytometry assay. Enzyme-linked immunosorbent assay was used to detect the level of cytokines.

RESULTS:

Zymosan-A protected mice from radiation-induced death and prevented radiation-induced hematopoietic system damage. Zymosan-A also promoted cell viability and inhibited cell apoptosis caused by radiation, induced radioprotective effects via TLR2, upregulated IL-6, IL-11, IL-12, and TNF-α in vivo.

CONCLUSION:

Zymosan-A can provide protection against radiation-induced hematopoietic system damage by targeting the TLR2 signaling pathway. Thus, Zymosan-A can be potentially effective radioprotectant.
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Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Protectores contra Radiación / Zimosan / Receptor Toll-Like 2 / Sistema Hematopoyético Límite: Animals Idioma: En Revista: Cell Physiol Biochem Asunto de la revista: BIOQUIMICA / FARMACOLOGIA Año: 2017 Tipo del documento: Article

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Protectores contra Radiación / Zimosan / Receptor Toll-Like 2 / Sistema Hematopoyético Límite: Animals Idioma: En Revista: Cell Physiol Biochem Asunto de la revista: BIOQUIMICA / FARMACOLOGIA Año: 2017 Tipo del documento: Article