Regulation of Autophagy Affects the Prognosis of Mice with Severe Acute Pancreatitis
| Autor: | Liang Xia, Nonghua Lu, Yaobin Ouyang, Xiaoyu Yang, Jianhua Wan, Yin Zhu, Jie Chen, Dangyan Wu |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Lipopolysaccharide Physiology Interleukin-1beta Pharmacology medicine.disease_cause Proinflammatory cytokine 03 medical and health sciences chemistry.chemical_compound Mice Internal medicine Autophagy Medicine Animals Inflammation Mice Inbred BALB C business.industry Pancreatitis Acute Necrotizing Adenine Caspase 1 Gastroenterology NF-kappa B Hepatology medicine.disease Prognosis Disease Models Animal Oxidative Stress 030104 developmental biology Treatment Outcome chemistry Acute pancreatitis Signal transduction business Flux (metabolism) Oxidative stress Signal Transduction |
| Zdroj: | Digestive diseases and sciences. 63(10) |
| ISSN: | 1573-2568 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full text from SpringerLink