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Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway

机译:黄ical苷通过腺苷A2a受体相关的TGF-β1诱导的ERK1 / 2信号通路减轻博来霉素诱导的肺纤维化

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摘要

BackgroundBaicalin has been reported to have anti-fibrosis effect; however, its mechanism still remains to be elucidated. Adenosine A2a receptor (A2aR) is a novel inflammation regulator, and transforming growth factor-β1 (TGF-β1)-induced extracellular signal regulated kinase1/2 (ERK1/2) signaling pathway plays an important role in idiopathic pulmonary fibrosis (IPF). This study was to explore the relationship of A2aR and TGF-β1-induced ERK1/2 in bleomycin (BLM)-induced pulmonary fibrosis in mice, and to investigate whether A2aR mediate the anti-fibrosis effect of Baicalin on BLM-induced pulmonary fibrosis.
机译:背景有报道称黄been苷具有抗纤维化作用。然而,其机制仍有待阐明。腺苷A2a受体(A2aR)是一种新型的炎症调节剂,而转化生长因子-β1(TGF-β1)诱导的细胞外信号调节激酶1/2(ERK1 / 2)信号通路在特发性肺纤维化(IPF)中起着重要作用。本研究旨在探讨博莱霉素(BLM)诱导的小鼠肺纤维化中A2aR和TGF-β1诱导的ERK1 / 2的关系,并探讨A2aR是否介导黄ical苷对BLM诱导的肺纤维化的抗纤维化作用。

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