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Copyright © 2021 Yingying Lu et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0/

Abstract

Background and Purpose. Previous studies showed that Maresin1 (MaR1), one of the metabolites from docosahexaenoic acid (DHA), could alleviate acute inflammation and prompt inflammation resolution. Also, it attenuated pancreatic injury in caerulein-induced acute pancreatitis (AP) in mice. However, the mechanisms underlying this suppression of inflammation and AP remain unknown. Method. Repeated caerulein injection was used to induce AP and chronic pancreatitis (CP) models in mice. The histopathological and serological changes were examined for evaluating the severity of the AP model, and flow cytometry was used for detecting macrophage phagocytosis and phenotype. Meanwhile, clodronate liposomes were used for macrophage depletion in mice. Finally, the CP model was adopted to further observe the protective effect of MaR1. Result. MaR1 administration manifested the improved histopathological changes and the lower serum levels of amylase and lipase. However, MaR1 played no protective role in the pancreatic acinar cell line in vitro. It obviously reduced the macrophage infiltration in the injured pancreas, especially M1-type macrophages. After macrophage clearance, MaR1 showed no further protection in vivo. This study also demonstrated that MaR1 could alleviate fibrosis to limit AP progression in the CP model. Conclusion. Our data suggests that MaR1 was a therapeutic and preventive target for AP in mice, likely operating through its effects on decreased macrophage infiltration and phenotype switch.

Details

Title
The Proresolving Lipid Mediator Maresin1 Alleviates Experimental Pancreatitis via Switching Macrophage Polarization
Author
Lu, Yingying 1   VIAFID ORCID Logo  ; Lu, Guotao 2   VIAFID ORCID Logo  ; Gao, Lin 3 ; Zhu, Qingtian 2 ; Xue, Jing 4 ; Zhang, Jingzhu 3 ; Ma, Xiaojie 3 ; Ma, Nan 3 ; Yang, Qi 3 ; Dong, Jie 3 ; Gong, Weijuan 2 ; Li, Weiqin 5   VIAFID ORCID Logo  ; Tong, Zhihui 5   VIAFID ORCID Logo 

 Department of Surgical Intensive Care Unit (SICU), Department of General Surgery, Jinling Hospital, Medical School of Southeast University, No. 305 Zhongshan East Road, Nanjing, 210002 Jiangsu, China 
 Pancreatic Center, Department of Gastroenterology, Affiliated Hospital of Yangzhou University, No. 368 Hanjiang Media Road, Yangzhou, 225000 Jiangsu, China 
 Surgical Intensive Care Unit (SICU), Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, No. 305 Zhongshan East Road, Nanjing, 210002 Jiangsu, China 
 State Key Laboratory of Oncogenes and Related Genes, Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China 
 Department of Surgical Intensive Care Unit (SICU), Department of General Surgery, Jinling Hospital, Medical School of Southeast University, No. 305 Zhongshan East Road, Nanjing, 210002 Jiangsu, China; Surgical Intensive Care Unit (SICU), Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, No. 305 Zhongshan East Road, Nanjing, 210002 Jiangsu, China 
Editor
Rômulo Dias Novaes
Publication year
2021
Publication date
2021
Publisher
John Wiley & Sons, Inc.
ISSN
09629351
e-ISSN
14661861
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2503350998
Copyright
Copyright © 2021 Yingying Lu et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0/