TLR4型
MAPK/ERK通路
肿瘤坏死因子α
化学
信号转导
蛋白激酶A
NF-κB
磷酸化
激酶
细胞生物学
分泌物
HMGB1
癌症研究
受体
生物化学
生物
免疫学
作者
Zhanchi Xu,Ruyi Lin,Xuenan Hou,Jun Wu,Weibo Zhao,Huanhuan Ma,Ziying Fan,Shijie Li,Yuan Zhu,Danyan Zhang
标识
DOI:10.1016/j.ijbiomac.2020.09.035
摘要
The immunomodulatory effect of a novel purified polysaccharide (JCH-1) isolated from Isaria cicadae Miquel had been confirmed to promote secretion of nitric oxide (NO), tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6) in our previous study. However, the immunomodulatory mechanism was still unclear. The purpose of this study was to investigate the immunomodulatory mechanism of JCH-1. Experimental data showed that JCH-1 could increase protein expression of toll-like receptor 4 (TLR4), promote the phosphorylation of mitogen-activated protein kinase (MAPK), as well as nuclear factor-kappa B (NF-κB) p65. Importantly, TLR4 inhibitor inhibited JCH-1-induced activation of MAPK-NF-κB signaling pathway, thus suppressed JCH-1-induced secretion of NO, TNF-α and IL-6. Collectively, these results indicated that JCH-1 actives RAW264.7 cells through TLR4-MAPK-NF-κB signaling pathway.
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