Elevated Level of miR‐711 Is Associated With Inflammation and Disease Progression in Patients With Severe Acute Pancreatitis

急性胰腺炎 炎症 氧化应激 活力测定 下调和上调 胰腺炎 p38丝裂原活化蛋白激酶 免疫学 促炎细胞因子 生物 癌症研究 MAPK/ERK通路 炎症反应 胰腺疾病 细胞 生物标志物 信号转导 病理生理学 内科学 体外 医学 细胞培养 胃肠病学
作者
Huili Chen,Changjing Qu,Xiufeng Pang,Xuan Wang,Ju Tian,Zhihua Tao,Feng Zhu
出处
期刊:Microbiology and Immunology [Wiley]
标识
DOI:10.1111/1348-0421.70044
摘要

Severe acute pancreatitis (SAP) is a critical abdominal emergency, with inflammatory response being the core pathogenic mechanism. This study aims to explore the role of miR-711 in SAP and its underlying mechanisms. This study enrolled 121 MAP patients and 109 SAP patients, collecting their clinical data. qRT-PCR measured miR-711 expression in serum and cells. Cell viability was tested with CCK-8, inflammatory factors via ELISA kits, and oxidative stress using SOD and MDA kits. The dual-luciferase assay confirmed miR-711 and KRT8 binding. Compared to the mild acute pancreatitis (MAP) group, the expression level of miR-711 in the serum of patients in the SAP group was significantly upregulated and positively correlated with relevant indicators. The ROC curve demonstrated its potential diagnostic value for SAP. In vitro, the miR-711 inhibitor effectively enhances the viability of Caerulein-induced AR42J cells and alleviates their inflammation and oxidative damage. Furthermore, the study confirmed that KRT8 is a downstream target gene of miR-711, and there is a negative correlation between their expressions. KRT8 may reverse the protective effect of miR-711 inhibitor on Cerulein-induced AR42J cells by regulating the NF-κB and p38 MAPK signaling pathways. The serum level of miR-711 in SAP patients is significantly upregulated and negatively correlated with SAP disease-related indicators. In vitro models demonstrate that inhibition of miR-711 effectively alleviates cerulein-induced cellular damage. Overexpression of KRT8 can reverse the cellular damage caused by miR-711 overexpression.
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