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首页> 外文期刊>The Journal of Nutritional Biochemistry >Synergistic effect of natural compounds on the fatty acid-induced autophagy of activated hepatic stellate cells
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Synergistic effect of natural compounds on the fatty acid-induced autophagy of activated hepatic stellate cells

机译：天然化合物对脂肪酸诱导的肝星状细胞自噬的协同作用

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摘要

Autophagy, a lysosomal pathway to maintain cellular homeostasis, is mediated via the mammalian target of rapamycin (mTOR)-dependent pathways. Hepatic stellate cells (HSCs), previously termed fat- or vitamin A-storing cells, can transdifferentiate into myofibroblast-like cells and are the most relevant cell type for overproduction of extracellular matrix (ECM) and development of liver fibrosis during injury. However, the role of autophagy in fat metabolism of HSCs remains unclear. This study investigates the regulatory effect of natural compounds on fatty acid-induced autophagy pathways of nonchemical-induced HSC (NHSC) and thioacetamide-induced HSC. Oleic acid (OA) and palmitic acid (PA) have shown a significant effect on cell proliferation with oil red O staining and Western blot confirming that OA and PA induce fat storage ability and autophagy protein expression in NHSC. Natural compounds rutin, curcumin, antroquinonol and benzyl cinnamate treatment have shown no effect on the autophagy protein expression. Nevertheless, cells pretreated with OA and PA then treated with rutin, curcumin, antroquinonol and benzyl cinnamate could significantly induce the light chain I/II (LC3 I/II) protein expression. In mTOR-dependent pathway, the PI3K-Class I, Akt, and p-mTOR proteins were decreased with PA treatment. However, there were no significant changes in PI3K-Class III and Beclin-1 protein expressions found to imply that this autophagy is unrelated to the mTOR-independent pathway. Taken together, the present study unveils rutin and curcumin as a possible effective stimulation for fatty acid-induced autophagy via mTOR-dependent pathways in NHSC. We further suggest the benefits of these natural compounds for alleviating liver fibrosis. (C) 2014 Elsevier Inc. All rights reserved.
机译：自噬是维持细胞稳态的溶酶体途径，是通过哺乳动物雷帕霉素靶标（mTOR）依赖性途径介导的。以前称为脂肪或维生素A储存的肝星状细胞（HSC）可以分化为成肌纤维母细胞样细胞，并且是细胞外基质（ECM）过量生产和损伤过程中肝纤维化发展最相关的细胞类型。然而，自噬在HSCs脂肪代谢中的作用仍不清楚。这项研究调查了天然化合物对非化学诱导的HSC（NHSC）和硫代乙酰胺诱导的HSC的脂肪酸诱导的自噬途径的调节作用。油酸（OA）和棕榈酸（PA）通过油红O染色和Western印迹显示出对细胞增殖的显着影响，证实了OA和PA可以诱导NHSC的脂肪储存能力和自噬蛋白表达。天然化合物芦丁，姜黄素，抗喹诺酮和肉桂酸肉桂酯处理对自噬蛋白表达没有影响。然而，用OA和PA预处理的细胞然后用芦丁，姜黄素，蒽醌和肉桂酸肉桂酯处理的细胞可以显着诱导轻链I / II（LC3 I / II）蛋白表达。在mTOR依赖性途径中，PA处理可降低PI3K-Class I，Akt和p-mTOR蛋白。但是，没有发现PI3K-Class III和Beclin-1蛋白表达有明显变化，这表明这种自噬与mTOR非依赖性途径无关。综上所述，本研究揭示了芦丁和姜黄素作为通过NHSC中mTOR依赖性途径对脂肪酸诱导的自噬的有效刺激。我们进一步建议这些天然化合物对减轻肝纤维化的益处。 （C）2014 Elsevier Inc.保留所有权利。

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