Emodin Alleviates Intestinal Barrier Dysfunction by Inhibiting Apoptosis and Regulating the Immune Response in Severe Acute Pancreatitis
| Autor: | Wenjing Wu, Xueying Shi, Bing Qi, Qi Zhou, Hong Xiang, Wenhui Guo, Wenhui Liu, Zhengpeng Wang, Shilin Xia, Jiacheng Zou, Wan Xueting, Han Liu, Dong Shang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Emodin
Lipopolysaccharide Endocrinology Diabetes and Metabolism IL-1β - interleukin 1β Caspase 3 Pharmacology HE - hematoxylin and eosin chemistry.chemical_compound Mice Endocrinology Immune system SIRS - systemic inflammatory response syndrome Internal Medicine medicine AP - acute pancreatitis Animals Intestinal Mucosa ELISA - enzyme-linked immunosorbent assay Hepatology apoptosis Original Articles medicine.disease SAP - severe acute pancreatitis ZO-1 - Zonula occludens 1 Disease Models Animal chemistry Pancreatitis Apoptosis MLN - mesenteric lymph node cells ComputingMethodologies_DOCUMENTANDTEXTPROCESSING intestinal dysfunction Acute pancreatitis TNF-α - tumor necrosis factor α Interleukin 17 Signal transduction inflammatory immune response severe acute pancreatitis |
| Zdroj: | Pancreas |
| ISSN: | 1536-4828 0885-3177 |
| Popis: | Supplemental digital content is available in the text. Objective The intestinal barrier injury caused by severe acute pancreatitis (SAP) can induce enterogenous infection, further aggravating the inflammatory reactions and immune responses. This study aimed to test the hypothesis that emodin protects the intestinal function and is involved in the immune response in SAP. Methods The network pharmacology was established using the Swiss target prediction and pathway enrichment analysis. The SAP mice model was induced by cerulein (50 μg/kg) and lipopolysaccharide (10 mg/kg) hyperstimulation. The pharmacological effect of emodin in treating SAP was evaluated at mRNA and protein levels by various methods. Results The network analysis provided the connectivity between the targets of emodin and the intestinal barrier–associated proteins and predicted the BAX/Bcl-2/caspase 3 signaling pathway. Emodin alleviated the pathological damages to the pancreas and intestine and reduced the high concentrations of serum amylase and cytokines in vivo. Emodin increased the expression of intestinal barrier–related proteins and reversed the changes in the apoptosis-related proteins in the intestine. Simultaneously, emodin regulated the ratio of T helper type 1 (TH1), TH2, TH17, γδ T cells, and interferon γ/interleukin 17 producing γδ T cells. Conclusions These findings partly verified the mechanism underlying the regulation of the intestinal barrier and immune response by emodin. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|