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.
Highlights
Acute pancreatitis (AP) is one of the common acute abdominal fatal diseases
Our group previously reported that docosahexaenoic acid (DHA) exerted a protective effect on acute pancreatitis (AP)
This study investigated the effect of MaR1 to partly explain its clinical benefit
Summary
Acute pancreatitis (AP) is one of the common acute abdominal fatal diseases. Severe AP (SAP) accounts for about 15%20% of patients with AP and develops approximately 30% mortality [1, 2]. The prognosis of AP is related to an excessive inflammatory response In this process, deregulated immune cells mediate the inflammatory cascade, leading to systemic inflammatory response syndrome and multiple organ failure [3]. Excessive inflammation may lead to injury in normal tissues and develop into chronic diseases [2, 13]. Maresin (7,14-dihydroxydocosa-4Z, 8Z,10,12,16Z,19Z-hexaenoic acid, MaR1) has been shown to be a potent mediator to inhibit neutrophil infiltration, promote macrophage efferocytosis, and enhance tissue regeneration in acute inflammation [18,19,20]. Several studies reported the protective effects of MaR1 on AP without clarifying its specific target cells [24, 25]. The purpose of this study was to verify the hypothesis of whether MaR1 could protect against AP, as well as exploring the possible underlying mechanism
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