The Proresolving Lipid Mediator Maresin1 Alleviates Experimental Pancreatitis via Switching Macrophage Polarization

  • Mediators Inflamm. 2021 Mar 9:2021:6680456. doi: 10.1155/2021/6680456.
Yingying Lu  1 ,  Guotao Lu  2 ,  Lin Gao  3 ,  Qingtian Zhu  2 ,  Jing Xue  4 ,  Jingzhu Zhang  3 ,  Xiaojie Ma  3 ,  Nan Ma  3 ,  Qi Yang  3 ,  Jie Dong  3 ,  Weijuan Gong  2 ,  Weiqin Li  1  3 ,  Zhihui Tong  1  3
Affiliations
  • 1. 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.
  • 2. Pancreatic Center, Department of Gastroenterology, Affiliated Hospital of Yangzhou University, No. 368 Hanjiang Media Road, Yangzhou, 225000 Jiangsu, China.
  • 3. 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.
  • 4. 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.
PMID: 33776575 DOI: 10.1155/2021/6680456
Abstract

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.

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