Caffeine inhibits hypoxia-induced renal fibroblast activation by antioxidant mechanism.

IF 3.3 3区 生物学 Q3 CELL BIOLOGY
Angkhana Nilnumkhum, Rattiyaporn Kanlaya, Sunisa Yoodee, Visith Thongboonkerd
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引用次数: 25

Abstract

Caffeine has been demonstrated to possess anti-fibrotic activity against liver fibrosis. However, its role in renal fibrosis remained unclear. This study investigated the effects of caffeine on renal fibroblast activation induced by hypoxia (one of the inducers for renal fibrosis). BHK-21 fibroblasts were cultured under normoxia or hypoxia with or without caffeine treatment. Hypoxia increased levels of fibronectin, α-smooth muscle actin, actin stress fibers, intracellular reactive oxygen species (ROS), and oxidized proteins. However, caffeine successfully preserved all these activated fibroblast markers to their basal levels. Cellular catalase activity was dropped under hypoxic condition but could be reactivated by caffeine. Hif1a gene and stress-responsive Nrf2 signaling molecule were elevated/activated by hypoxia, but only Nrf2 could be partially recovered by caffeine. These data suggest that caffeine exhibits anti-fibrotic effect against hypoxia-induced renal fibroblast activation through its antioxidant property to eliminate intracellular ROS, at least in part, via downstream catalase and Nrf2 mechanisms.

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咖啡因通过抗氧化机制抑制缺氧诱导的肾成纤维细胞活化。
咖啡因已被证明对肝纤维化具有抗纤维化活性。然而,其在肾纤维化中的作用尚不清楚。本研究探讨了咖啡因对缺氧诱导的肾成纤维细胞活化的影响(肾纤维化的诱导剂之一)。将BHK-21成纤维细胞分别培养于常氧或缺氧条件下,并分别添加或不添加咖啡因。缺氧增加了纤维连接蛋白、α-平滑肌肌动蛋白、肌动蛋白应激纤维、细胞内活性氧(ROS)和氧化蛋白的水平。然而,咖啡因成功地将所有这些激活的成纤维细胞标记物保持在其基础水平。细胞过氧化氢酶活性在缺氧条件下下降,但咖啡因可以使其重新激活。缺氧使Hif1a基因和应激反应性Nrf2信号分子升高/激活,但咖啡因只能部分恢复Nrf2。这些数据表明,咖啡因通过其抗氧化特性消除细胞内ROS,至少部分通过下游过氧化氢酶和Nrf2机制,对缺氧诱导的肾成纤维细胞活化具有抗纤维化作用。
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来源期刊
CiteScore
6.40
自引率
0.00%
发文量
7
审稿时长
53 weeks
期刊介绍: Cell Adhesion & Migration is a multi-disciplinary, peer reviewed open access journal that focuses on the biological or pathological implications of cell-cell and cell-microenvironment interactions. The main focus of this journal is fundamental science. The journal strives to serve a broad readership by regularly publishing review articles covering specific disciplines within the field, and by publishing focused issues that provide an overview on specific topics of interest within the field. Cell Adhesion & Migration publishes relevant and timely original research, as well as authoritative overviews, commentaries, and perspectives, providing context for the work presented in Cell Adhesion & Migration and for key results published elsewhere. Original research papers may cover all topics important in the field of cell-cell and cell-matrix interactions. Cell Adhesion & Migration also publishes articles related to cell biomechanics, biomaterial, and development of related imaging technologies.
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