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首页> 外文期刊>Parasitology >Paeoniflorin attenuates schistosomiasis japonica-associated liver fibrosis through inhibiting alternative activation of macrophages.
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Paeoniflorin attenuates schistosomiasis japonica-associated liver fibrosis through inhibiting alternative activation of macrophages.

机译：eon药苷通过抑制巨噬细胞的选择性激活来减轻日本血吸虫病相关的肝纤维化。

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摘要

Interleukin (IL)-13 and alternatively activated macrophages (AAMs) play an important role in liver granuloma and fibrosis of schistosomiasis. Paeoniflorin (PAE, C23H28O11) has been reported to have an anti-hepatic fibrosis effect in schistosomiasis; however, the mechanism has not been fully elucidated. In this study, we measured serum hyaluronic acid (HA) concentrations, liver granuloma diameter and volume density, fibrosis degree and expressions of IL-13, arginase-1 (ARG-1), nitric oxide synthase-2 (NOS-2), and phosphorylated signal transducer and activator of transcription 6 (p-STAT6) in mice liver of schistosomiasis. Then we detected expressions of specific biomarkers of AAMs and activity of Arg-1 in Kupffer cells (KCs) from infected and PAE-treated mice, or in KCs from uninfected mice, but exposed to rIL-13 in vitro. Finally, we observed expression of IL-13 signalling molecules in KCs and secretion of IL-13 from lymphocytes of infected and PAE-treated mice. Our results showed that during schistosomiasis, IL-13 expression and secretion increased with liver macrophages activated alternatively. PAE not only directly inhibited alternative activation of macrophages via reducing the phosphorylations of janus-activated kinase 2 (JAK2) and/or STAT6, leading to reduction of AAMs-related markers and Arg-1 activity, but also indirectly suppressed alternative activation of macrophages through decreasing secretion of IL-13. PAE might be a promising prophylactic agent for hepatic granuloma and fibrosis of schistosomiasis japonica.
机译：白介素（IL）-13和其他活化的巨噬细胞（AAM）在肝肉芽肿和血吸虫病纤维化中起重要作用。据报道eon药苷（PAE，C23H28O11）在血吸虫病中具有抗肝纤维化作用。但是，该机制尚未完全阐明。在这项研究中，我们测量了血清透明质酸（HA）的浓度，肝肉芽肿直径和体积密度，纤维化程度以及IL-13，精氨酸酶1（ARG-1），一氧化氮合酶2（NOS-2）的表达，血吸虫病小鼠肝脏中的磷酸化信号转导子和转录激活子6（p-STAT6）。然后，我们检测了感染和PAE处理小鼠的Kupffer细胞（KCs）或未感染小鼠的KCs中AAM特异性生物标志物的表达和Arg-1的活性，但它们在体外暴露于rIL-13。最后，我们观察到IL-13信号分子在KCs中的表达以及感染和PAE处理的小鼠淋巴细胞中IL-13的分泌。我们的结果表明，在血吸虫病期间，IL-13的表达和分泌随着肝巨噬细胞的交替激活而增加。 PAE不仅通过减少janus活化激酶2（JAK2）和/或STAT6的磷酸化来直接抑制巨噬细胞的替代活化，从而导致AAMs相关标志物和Arg-1活性的降低，而且通过以下方式间接抑制了巨噬细胞的替代活化： IL-13分泌减少。 PAE可能是日本血吸虫病肝肉芽肿和纤维化的有希望的预防剂。

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