Abstract
Objective To study the effect of ERCP on acute pancreatitis in rats and its effect on reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK) pathway. Methods 60 male rats were divided into blank group (intravenous injection of 0.1 ml volume fraction of 0.1% fetal bovine serum), model group (intravenous injection of 0.1 ml volume fraction of 0.1% fetal bovine serum) and surgical intervention group (endoscopic retrograde cholangiopancreatography) (n=20). After the rats were killed, the peripheral blood and pancreatic tissues were collected and the nuclear translocation of nuclear factor-κB (NF-κB) was detected by immunohistochemistry. The serum levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-1 β in rat serum were determined by hematoxylin and eosin (HE) staining and flow cytometry respectively. The changes of p-JNK-JNK in pancreatic tissue were detected by flow cytometric analysis. The changes of p-JNK-JNK were detected by Western blotting method. Results Compared with the model group (35.9±2.2, 79.6±12.6, 322.3±28.5, 436.8±32.9), the NF-κB, ROS, p-JNK, JNK of the operation intervention group (12.3±1.1, 61.2±13.2, 2551.4±25.9, 289.6±36.5) obviously reduced (P=0.011, 0.015, 0.014, 0.009). Compared with the model group (85.6±2.5, 58.6±13.6, 82.3±12.5), the level of TNF-α, IL-6 and IL-1 β of surgical intervention group (22.3±1.1, 10.3±1.2, 11.3±2.3) obviously reduced (P=0.018, 0.012, 0.016). Conclusion The activation of the ROS/JNK pathway may cause a series of inflammatory reactions to aggravate the condition. Endoscopic retrograde cholangiopancreatography plays a role in the treatment of acute pancreatitis rats by inhibiting the ROS/JNK pathway. Key words: Acute pancreatitis; Endoscopic retrograde cholangiopancreatography; Reactive oxygen species/c-Jun N-terminal kinase pathway; Inflammatory response
Published Version
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