封堵器
MAPK/ERK通路
p38丝裂原活化蛋白激酶
TLR4型
信号转导
NF-κB
细胞生物学
下调和上调
促炎细胞因子
肿瘤坏死因子α
体内
化学
炎症
炎症性肠病
紧密连接
生物
免疫学
医学
生物化学
内科学
基因
疾病
作者
Shengwei Chen,Yi Zhang,Xueting Niu,Sahar Ghulam Mohyuddin,Jiayin Wen,Minglong Bao,Tianyue Yu,Lianyun Wu,Canyin Hu,Yanhong Yong,Xiaoxi Liu,A.M. Abd El‐Aty,Xingrong Ju
标识
DOI:10.3389/fnut.2021.748118
摘要
Herein, we assessed the anti-inflammatory and intestinal barrier protective effects of butyrolactone-I (BTL-1), derived from the coral-derived endophytic fungus (Aspergillus terreus), using the LPS-induced IPEC-J2 inflammation model and the DSS-induced IBD model in mice. In IPEC-J2 cells, pretreatment with BTL-I significantly inhibited TLR4/NF-κB signaling pathway and JNK phosphorylation, resulting in the decrease of IL-1β and IL-6 expression. Interestingly, BTL-1 pretreatment activated the phosphorylation of ERK and P38, which significantly enhanced the expression of TNF-α. Meanwhile, BTL-1 pretreatment upregulated tight junction protein expression (ZO-1, occludin, and claudin-1) and maintained intestinal barrier and intestinal permeability integrity. In mice, BTL-1 significantly alleviated the intestinal inflammatory response induced by DSS, inhibited TLR4/NF-κB signaling pathway, and MAPK signaling pathway, thus reducing the production of IL-1, IL-6, and TNF-α. Further, the expression of tight junction proteins (ZO-1, occludin, and claudin-1) was upregulated in BTL-1 administrated mice. Therefore, it has been suggested that butyrolactone-I alleviates inflammatory responses in LPS-stimulated IPEC-J2 and DSS-induced murine colitis by TLR4/NF-κB and MAPK signal pathway. Thereby, BTL-1 might potentially be used as an ocean drug to prevent intestinal bowel disease.
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