Quercetin inhibits caerulein-induced acute pancreatitis through regulating miR-216b by targeting MAP2K6 and NEAT1
| Autor: | Bo Sheng, Wei Chen, Yang Liu, Lei Zhao, Jie Zhen, Weishuai Bian, Xuefeng Zang |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
TRAF2 p38 mitogen-activated protein kinases Immunology Cell Down-Regulation Endogeny Inflammation MAP Kinase Kinase 6 Pharmacology p38 Mitogen-Activated Protein Kinases MAP2K6 Cell Line Mice 03 medical and health sciences 0302 clinical medicine medicine Animals Pharmacology (medical) Pancreas Competing endogenous RNA Chemistry medicine.disease Rats Up-Regulation Mice Inbred C57BL Disease Models Animal MicroRNAs 030104 developmental biology medicine.anatomical_structure Pancreatitis Acute pancreatitis Quercetin RNA Long Noncoding medicine.symptom Ceruletide 030217 neurology & neurosurgery Signal Transduction |
| Zdroj: | Inflammopharmacology. 29:549-559 |
| ISSN: | 1568-5608 0925-4692 |
| Popis: | Acute pancreatitis (AP) is a common acute abdominal disease with high mortality and mortality rates. Increasing evidences clarified that Traditional Chinese Medicine (TCM) adjuvant therapy for AP can be used and it gives a positive effect. Quercetin (3,3',4',5,7-pentahydroxyflavone, QE) is a type of flavone compound with positive effect on cancer and inflammation prevention. The current study aims to identify the effect of QE on AP and potential molecular effect. In this case, caerulein (CAE) induced AP cell and mice model were used. QE alleviated inflammatory mediators TNF-α, IL-6, and IL-10 in experiments. In addition, miR-216b was increased based on QE treatment. In further study, MAP2K6 of p38/MAPK signaling pathway was identified as a direct target of miR-216b, and QE inhibited p38/MAPK signaling pathway through up-regulating miR-216b. Our study also first confirmed that long non-coding RNA NEAT1 is a direct target of miR-216b and can be suppressed by QE. Because of the target, NEAT1, miR-216b, and MAP2K6 formed a competitive endogenous RNA (ceRNA) network. Besides direct target mediated by QE, it also decreased TNF-α which down-regulated TRAF2 and MAP3K5 located on upstream of p38/MAPK signaling and formed a feedback loop. In conclusion, QE has a protective effect on AP through inhibiting p38/MAPK signaling pathway by up-regulating miR-216b and suppressing TNF-α. |
| Databáze: | OpenAIRE |
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