Abstract：
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.
摘要：
茶氨酸是茶叶中的一种天然生物活性成分，具有抗炎作用。本研究旨在探讨茶氨酸对脂多糖(LPS)诱导的IPEC-J2细胞肠紧密连接损伤的影响及其机制。结果表明，LPS通过增加活性氧的产生和乳酸脱氢酶（LDH）的释放以及降低紧密连接蛋白相关基因zonulaoccludens-1（ZO-1，也称为Tjp1）的mRNA表达来诱导紧密连接损伤。Occludin和Claudin-1，而L-茶氨酸逆转了这种作用，并减弱了p38丝裂原活化蛋白激酶（p38MAPK）mRNA表达的增加。p38MAPK抑制剂（SB203580）减弱了核苷酸结合寡聚化结构域样受体家族pyrin结构域包含3（Nlrp3）炎症小体和白介素1β（IL-1β）的mRNA表达，并增加了Tjp1，Occludin和Claudin-1的mRNA表达，与L-茶氨酸具有相似的作用。此外,NLRP3抑制剂MCC950减弱了Il-1β表达和LDH释放，同时增加紧密连接蛋白相关基因的表达。总之,L-茶氨酸可能通过抑制p38MAPK介导的NLRP3炎性体通路的激活来保护LPS诱导的肠紧密连接损伤。
