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
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI