封堵器
紧密连接
炎症体
p38丝裂原活化蛋白激酶
细胞生物学
MAPK/ERK通路
脂多糖
化学
蛋白激酶A
吡喃结构域
分子生物学
生物
信号转导
激酶
生物化学
受体
免疫学
作者
Xiaoling Chen,Diaoyun Luo,Gang Jia,Hua Zhao,Guangmang Liu,Zhiqing Huang
标识
DOI:10.1016/j.fct.2023.113870
摘要
L-theanine is a natural bioactive component in tea leaves and has anti-inflammatory effects. The study aimed to investigated the effects and underlying mechanisms of L-theanine on lipopolysaccharide (LPS)-induced intestinal tight junction damage in IPEC-J2 cells. Results showed that LPS induced tight junction damage by increasing reactive oxygen species production and lactate dehydrogenase (LDH) release and decreasing the mRNA expression of tight junction proteins related genes zonula occludens-1 (ZO-1, also known as Tjp1), Occludin and Claudin-1, while L-theanine reversed such an effect and attenuated the increase of p38 mitogen-activated protein kinase (p38 MAPK) mRNA expression. The p38 MAPK inhibitor (SB203580) attenuated the mRNA expression of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (Nlrp3) inflammasome and interleukin-1β (Il-1β), and increased the mRNA expression of Tjp1, Occludin and Claudin-1, which showed a similar effect with L-theanine. In addition, NLRP3 inhibitor MCC950 attenuated the Il-1β expression and LDH release, while increased the expression of tight-junction protein-related genes. In conclusion, L-theanine could protect LPS-induced intestinal tight junction damage by inhibiting the activation of p38 MAPK-mediated NLRP3 inflammasome pathway.
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