AI Article Synopsis
- The study investigates how specific interleukin cytokines (IL-6, IL-17, IL-23, IL-23R) are involved in the development of acute pancreatitis in rat models.
- Thirty-six rats were divided into control, model, and intervention groups, with the latter two receiving an injection to induce pancreatitis, and one group receiving treatment simultaneously.
- Results showed significantly higher levels of IL-6, IL-17, and IL-23 in the model group compared to controls, indicating that IL-23 is an important mediator that facilitates the effects of IL-6 and IL-17 in promoting acute pancreatitis.
Article Abstract
Objective: To explore the molecular mechanism of interleukin cytokines IL-6, IL-17, IL-23, IL-23R in the onset of acute pancreatitis in rats pancreatitis models.
Methods: Thirty six SD rats were randomized into 3 groups: control group, model group, and intervention group (n = 12). The rats in model group and intervention group were induced by intraperitoneal injection of 1-arginine, and those in intervention group were treated by tail intravenous administration of drugs at the same time. Then the rats were sacrified at 3rd, 6th, and 12th h. after the modeling. The levels of IL-6 ,IL-17, IL-23, IL-23R in blood, pancreas, lung and kidney were checked by ELISA.
Results: The IL-6 levels of serum, pancreas, lung and kidney in AP Model group were obviously higher than those in the control group and intervention group. This trend increased with time. Similarly, the levels of IL-17 and IL-23 in AP group were obviously higher than those in the control group and intervention group. Compared with the control and intervention group, AP group showed higher IL-23R levels in serum, pancreas, but lower IL-23R levels in lung and kidney.
Conclusion: IL-23 is a mediator involved in the formation of IL-17 and IL-6, they all can promote acute pancreatitis.
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