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提取物通过抑制ROS/NLRP3/半胱天冬酶-1/白细胞介素-1信号轴对感染的GES-1细胞的抗炎作用。

The Anti-Inflammatory Effect of Extract on -Infected GES-1 Cells through the Inhibition of ROS/NLRP3/Caspase-1/IL-1 Signaling Axis.

作者信息

Li Lili, Bao Bo, Chai Xingxing, Chen Xiaoyu, Su Xiaohua, Feng Shixiu, Zhu Xiaohui

机构信息

Laboratory Animal Centre, Guangdong Medical University, Dongguan 523808, China.

Department of Pathophysiology, School of Basic Medicine Sciences, Guangdong Medical University, Zhanjiang 524023, China.

出版信息

Can J Infect Dis Med Microbiol. 2022 Jul 15;2022:5469236. doi: 10.1155/2022/5469236. eCollection 2022.

Abstract

() is the main pathogenic factor of gastric cancer, chronic gastritis, and other gastric diseases. It has been found that (CN) as an air-dried leaf extract has a broad-spectrum antibacterial effect. This study aims to examine the effect of CN on -infected GES-1 cells and elucidate its underlying mechanism by extracting active ingredients from air-dried leaves. GES-1 cells were cocultured with HPSS1 at MOI = 100 : 1 and treated with different concentrations of CN (100 and 200 g/ml). Results showed that CN can significantly reduce cellular LDH leakage and attenuate -induced cell apoptosis and ROS production in GSE-1 cells, so as to protect gastric epithelial cells from damage by . CN can also inhibit the secretion of inflammatory factors, such as TNF-, IL-1, IL-6, and IL-8. After CN treatment, the expression levels of active caspase-1, PYCARD, and NLRP3 were remarkably decreased in the treatment groups compared with the model group. To sum up, CN is highly protective against -induced cell damage and apoptosis; CN can depress NLRP3 inflammasome activation and ROS production via the ROS/NLRP3/caspase-1/IL-1 signaling axis to suppress -triggered inflammatory response and pyroptosis.

摘要

()是胃癌、慢性胃炎及其他胃部疾病的主要致病因素。研究发现,(CN)作为一种风干叶提取物具有广谱抗菌作用。本研究旨在通过从风干叶中提取活性成分,考察CN对感染的GES-1细胞的影响,并阐明其潜在机制。将GES-1细胞与HPSS1以MOI = 100∶1共培养,并用不同浓度的CN(100和200μg/ml)处理。结果表明,CN可显著降低细胞LDH泄漏,减轻感染诱导的GSE-1细胞凋亡和ROS产生,从而保护胃上皮细胞免受感染损伤。CN还可抑制TNF-、IL-1、IL-6和IL-8等炎性因子的分泌。与模型组相比,CN处理后各治疗组中活性caspase-1、PYCARD和NLRP3的表达水平显著降低。综上所述,CN对感染诱导的细胞损伤和凋亡具有高度保护作用;CN可通过ROS/NLRP3/caspase-1/IL-1信号轴抑制NLRP3炎性小体激活和ROS产生,从而抑制感染引发的炎症反应和细胞焦亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d894/9307406/6a8d9a6accbb/CJIDMM2022-5469236.001.jpg

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