Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, 17 Yongwaizheng Street, Nanchang, 330006, Jiangxi, People's Republic of China.
Dig Dis Sci. 2018 Oct;63(10):2639-2650. doi: 10.1007/s10620-018-5053-0. Epub 2018 Apr 9.
Acute pancreatitis (AP) is a common inflammatory disease that may develop to severe AP (SAP), resulting in life-threatening complications. Impaired autophagic flux is a characteristic of early AP, and its accumulation could activate oxidative stress and nuclear factor κB (NF-κB) pathways, which aggravate the disease process.
To explore the therapeutic effects of regulating autophagy after the onset of AP.
In this study, intraperitoneal injections of 3-methyladenine (3-MA) and rapamycin (RAPA) in the L-arginine or cerulein plus lipopolysaccharide (LPS) Balb/C mouse model. At 24 h after the last injection, pulmonary, intestinal, renal and pancreatic tissues were analyzed.
We found that 3-MA ameliorated systemic organ injury in two SAP models. 3-MA treatment impaired autophagic flux and alleviated inflammatory activation by modulating the NF-κB signaling pathway and the caspase-1-IL-1β pathway, thus decreasing the injuries to the organs and the levels of inflammatory cytokines.
Our study found that the regulation of autophagy could alter the progression of AP induced by L-arginine or cerulein plus LPS in mice.
急性胰腺炎（AP）是一种常见的炎症性疾病，可能发展为重症急性胰腺炎（SAP），导致危及生命的并发症。自噬通量的受损是早期 AP 的特征，其积累可能会激活氧化应激和核因子 κB（NF-κB）途径，从而加重疾病进程。
探讨 AP 发病后调节自噬的治疗效果。
在本研究中，采用腹腔内注射 3-甲基腺嘌呤（3-MA）和雷帕霉素（RAPA）在 L-精氨酸或亮抑蛋白酶原加脂多糖（LPS）Balb/C 小鼠模型中。在最后一次注射后 24 小时，分析肺、肠、肾和胰腺组织。
我们发现 3-MA 改善了两种 SAP 模型中的全身器官损伤。3-MA 治疗通过调节 NF-κB 信号通路和半胱天冬酶-1-IL-1β通路来损害自噬通量并减轻炎症激活，从而减少器官损伤和炎症细胞因子水平。
我们的研究发现，自噬的调节可以改变由 L-精氨酸或亮抑蛋白酶原加 LPS 诱导的小鼠 AP 的进展。
