Mechanism of the immunostimulatory activity by a polysaccharide from Dictyophora indusiata.

Autor: Deng C; Wuxi Medical School, Jiangnan University, Wuxi 214122, PR China; School of Pharmaceutics Science, Jiangnan University, Wuxi 214122, PR China., Shang J; School of Pharmaceutics Science, Jiangnan University, Wuxi 214122, PR China., Fu H; School of Pharmaceutics Science, Jiangnan University, Wuxi 214122, PR China., Chen J; School of Pharmaceutics Science, Jiangnan University, Wuxi 214122, PR China., Liu H; Wuxi Medical School, Jiangnan University, Wuxi 214122, PR China., Chen J; School of Pharmaceutics Science, Jiangnan University, Wuxi 214122, PR China. Electronic address: jhchenwhut@126.com.
Jazyk: angličtina
Zdroj: International journal of biological macromolecules [Int J Biol Macromol] 2016 Oct; Vol. 91, pp. 752-9. Date of Electronic Publication: 2016 Jun 09.
DOI: 10.1016/j.ijbiomac.2016.06.024
Abstrakt: Dictyophora indusiata, an edible mushroom, is widely used not only as health foods but also as traditional Chinese medicine. This study aimed to investigate the molecular mechanism involved in the immunostimulatory activity of a polysaccharide from Dictyophora indusiata (DIP) in RAW264.7 cells. Results indicated that DIP induced the up-regulation of nitric oxide (NO), interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumour necrosis factor (TNF-α) production as well as the mRNA expression levels of iNOS, IL-1β, IL-6 and TNF-α in macrophages. Furthermore, the functional blocking antibodies against TLR4 could markedly suppress DIP-mediated NO, IL-1β, IL-6 and TNF-α production. Flow cytometry and confocal laser-scanning microscopy analyses confirmed that DIP could bind specifically to target cells, and the binding could be inhibited by anti-TLR4 monoclonal antibodies. The expression of nuclear factor kappa B (NF-κB) p65 was significantly induced by DIP. Therefore, the DIP-induced macrophage activation may be mediated via the TLR4/NF-κB signalling pathway.
(Copyright © 2016 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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