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本文研究了胆囊收缩素(CCK)诱导的急性胰腺炎对ICR小鼠自发性活动自由节律的影响,分析生物节律与炎症性疾病及急性胰腺炎病理机制的相互关系。通过对全黑状态下的转轮甄别活动相和休息相行CCK诱导的急性胰腺炎造模,对比造模后的炎症程度以及两组前后周期、相位等节律指标的变化。结果发现相同剂量的急性胰腺炎ICR小鼠模型,休息相造模组比活动相造模组炎症程度重;且急性胰腺炎ICR小鼠活动节律的周期延长,在休息相造模组尤为明显。研究表明CCK诱导的急性胰腺炎可影响ICR小鼠的自由活动节律,且自由运转状态下不同相位造模时炎症轻重有明显区别,为急性胰腺炎重症化趋势的病理机制研究提供了可能的线索。
This article studies the effects of cholecystokinin (CCK) -induced acute pancreatitis on spontaneous activity free rhythm in ICR mice and the relationship between biorhythm and inflammatory diseases and the pathological mechanism of acute pancreatitis. CCK-induced acute pancreatitis model was established by round-robin screening and phase-shift in all-black state. The changes of inflammation after modeling and the change of rhythm and phase before and after the two groups were compared. The results showed that ICR mouse model at the same dose of acute pancreatitis, rest phase model group than the active phase model caused by the severity of inflammation; and acute pancreatitis ICR mouse activity rhythm of the cycle is prolonged, especially in rest phase modeling group. Studies have shown that CCK-induced acute pancreatitis can affect the free rhythm of ICR mice, and the free-running state of inflammation at different phases of significant differences in the severity of pathogenesis of severe pancreatitis aggravate the pathological mechanism provides a possible clues .