医学
胰腺炎
体内
巨噬细胞
巨噬细胞极化
吞噬作用
纤维化
药理学
病理
体外
免疫学
内科学
生物
生物化学
生物技术
作者
Yingying Lǚ,Guotao Lu,Lin Gao,Qingtian Zhu,Jing Xue,Jingzhu Zhang,Xiaojie Ma,Nan Ma,Qi Yang,Jie Dong,Weijuan Gong,Weiqin Li,Zhihui Tong
摘要
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.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.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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