绿原酸通过lncRNA GAS5/miR-23a/PTEN轴和p38丝裂原活化蛋白激酶途径促进自噬并减轻鼠伤寒沙门氏菌感染。

Chlorogenic Acid Promotes Autophagy and Alleviates Typhimurium Infection Through the lncRNAGAS5/miR-23a/PTEN Axis and the p38 MAPK Pathway.

作者信息

Tan Shirui, Yan Fang, Li Qingrong, Liang Yaping, Yu Junxu, Li Zhenjun, He Feifei, Li Rongpeng, Li Ming

机构信息

Center of Life Sciences, School of Life Sciences, Yunnan University, Kunming, China.

The Second Affiliated Hospital of Kunming Medical University, Kunming, China.

出版信息

Front Cell Dev Biol. 2020 Nov 5;8:552020. doi: 10.3389/fcell.2020.552020. eCollection 2020.

BACKGROUND

) causes several intestinal diseases. Polyphenols including chlorogenic acid (CGA) inhibit pathogenesis.

OBJECTIVE

This study aimed to investigate the mechanisms of CGA in infection.

METHODS

The intestinal pathological changes and survival rate of ST-infected mice were measured to verify the protection of CGA on infection. The antibacterial effects of CGA on the invasion to intestinal epithelial cells and autophagy was evaluated. The relationships among GAS5, miR-23a, and PTEN were verified. Expression of inflammation- and autophagy-related proteins was detected.

RESULTS

CGA treatment alleviated pathological damage, improved the secretion disturbance of intestinal cytokines caused by infection, and reduced the mortality of mice. Intestinal GAS5 was upregulated after CGA treatment. LncRNA GAS5 competitively bound to miR-23a to upregulate PTEN and inhibit the p38 MAPK pathway. CGA regulated the p38 MAPK pathway through lncRNA GAS5/miR-23a/PTEN axis to promote autophagy in infection. The functional rescue experiments of miR-23a and PTEN further identified these effects.

CONCLUSION

CGA promotes autophagy and inhibits infection through the GAS5/miR-23a/PTEN axis and the p38 MAPK pathway.

背景

（某种因素）会引发多种肠道疾病。包括绿原酸（CGA）在内的多酚类物质可抑制其发病机制。

目的

本研究旨在探究CGA在（某种感染）中的作用机制。

方法

检测感染（该病原体）的小鼠的肠道病理变化及存活率，以验证CGA对（该感染）的保护作用。评估CGA对（病原体）侵袭肠上皮细胞的抗菌作用及自噬情况。验证GAS5、miR-23a和PTEN之间的关系。检测炎症和自噬相关蛋白的表达。

结果

CGA处理减轻了病理损伤，改善了由（该感染）引起的肠道细胞因子分泌紊乱，并降低了小鼠死亡率。CGA处理后肠道GAS5上调。长链非编码RNA GAS5竞争性结合miR-23a以上调PTEN并抑制p38丝裂原活化蛋白激酶途径。CGA通过长链非编码RNA GAS5/miR-23a/PTEN轴调节p38丝裂原活化蛋白激酶途径，以促进（该感染）中的自噬。miR-23a和PTEN的功能挽救实验进一步证实了这些作用。