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首页> 外文期刊>Cell death & disease. >FABP4 contributes to renal interstitial fibrosis via mediating inflammation and lipid metabolism
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FABP4 contributes to renal interstitial fibrosis via mediating inflammation and lipid metabolism

机译：Fabp4通过介导炎症和脂质代谢促进肾间质纤维化有助于肾间质纤维化

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Fatty acid binding protein 4 (FABP4), a subtype of fatty acid-binding protein family, shows critical roles in metabolism and inflammation. However, its roles on regulating renal interstitial fibrosis (RIF) remain unclear. In this work, LPS-stimulated in vitro models on NRK-52E and NRK-49F cells, and in vivo UUO models in rats and mice were established. The results showed that comparing with control groups or sham groups, the expression levels of α-SMA, COL1A, COL3A, IL-1β, IL-6, and TNF-α in LPS-stimulated cells or UUO animals were significantly increased. Meanwhile, the levels of TC, TG, and free fatty acid were also significantly increased as well as the obvious lipid droplets, and the serum levels of BUN, Cr were significantly increased with large amounts of collagen deposition in renal tissues. Further investigation showed that compared with control groups or sham groups, the expression levels of FABP4 in LPS-stimulated cells and UUO animals were significantly increased, resulting in down- regulating the expression levels of PPARγ, upregulating the levels of p65 and ICAM-1, and decreasing the expression levels of ACADM, ACADL, SCP-2, CPT1, EHHADH, and ACOX1. To deeply explore the mechanism of FABP4 in RIF, FABP4 siRNA and inhibitor interfered cell models, and UUO model on FABP4 knockout (KO) mice were used. The results showed that the expression levels of α-SMA, COL1A, and COL3A were significantly decreased, the deposition of lipid droplets decreased, and the contents of TC, TG, and free fatty acids were significantly decreased after gene silencing. Meanwhile, the expression levels of PPAR-γ, ACADM, ACADL, SCP-2, CPT1, EHHADH, and ACOX1 were upregulated, the levels of p65 and ICAM-1 were downregulated, and the mRNA levels of IL-1β, IL-6, and TNF-α were decreased. Our results supported that FABP4 contributed to RIF via promoting inflammation and lipid metabolism, which should be considered as one new drug target to treat RIF.
机译：脂肪酸结合蛋白4（FABP4）是脂肪酸结合蛋白家族的亚型，表现出代谢和炎症的关键作用。然而，它对调节肾间质纤维化（RIF）的作用仍然不清楚。在这项工作中，建立了NRK-52E和NRK-49F细胞上的LPS刺激的体外模型，以及大鼠和小鼠的体内UUO模型。结果表明，与对照组或假组，α-SMA，COL1A，COL3A，IL-1β，IL-6和TNF-α的表达水平明显增加。同时，Tc，Tg和游离脂肪酸的水平也显着增加以及明显的脂液滴，并且肾组织中大量胶原沉积显着提高了明显的脂液体，Cr的血清水平。进一步的研究表明，与对照组或假组合相比，LPS刺激细胞和UUO动物中Fabp4的表达水平显着增加，导致降低PPARγ的表达水平，上调P65和ICAM-1的水平，并减少ACCM，ACADL，SCP-2，CPT1，EHHADH和ACOX1的表达水平。为了深深地探索RIF，Fabp4 siRNA和抑制剂干扰细胞模型中Fabp4的机制，使用Fabp4敲除（KO）小鼠的UUO模型。结果表明，在基因沉默后，脂肪液滴的沉积降低，​​脂液滴的沉积显着降低，脂质液滴的沉积和Tc，Tg和游离脂肪酸的含量显着降低。同时，PPAR-γ，ACCM，ACADL，SCP-2，CPT1，EHHADH和ACOX1的表达水平被上调，P65和ICAM-1的水平下调，IL-1β，IL-6的mRNA水平并且TNF-α降低。我们的结果支持FABP4通过促进炎症和脂质代谢的促进，这应该被认为是治疗RIF的一种新药靶标。

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