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芹菜素通过降低 caspase-3 激活和调节线粒体功能来保护内皮细胞免受脂多糖 (LPS) 诱导的炎症。

Apigenin protects endothelial cells from lipopolysaccharide (LPS)-induced inflammation by decreasing caspase-3 activation and modulating mitochondrial function.

机构信息

Department of Molecular Genetics, the Ohio State University, Columbus, OH 43210, USA.

出版信息

Int J Mol Sci. 2013 Aug 28;14(9):17664-79. doi: 10.3390/ijms140917664.

DOI:10.3390/ijms140917664
PMID:23989609
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3794747/
Abstract

Acute and chronic inflammation is characterized by increased reactive oxygen species (ROS) production, dysregulation of mitochondrial metabolism and abnormal immune function contributing to cardiovascular diseases and sepsis. Clinical and epidemiological studies suggest potential beneficial effects of dietary interventions in inflammatory diseases but understanding of how nutrients work remains insufficient. In the present study, we evaluated the effects of apigenin, an anti-inflammatory flavonoid abundantly found in our diet, in endothelial cells during inflammation. Here, we show that apigenin reduced lipopolysaccharide (LPS)-induced apoptosis by decreasing ROS production and the activity of caspase-3 in endothelial cells. Apigenin conferred protection against LPS-induced mitochondrial dysfunction and reestablished normal mitochondrial complex I activity, a major site of electron leakage and superoxide production, suggesting its ability to modulate endothelial cell metabolic function during inflammation. Collectively, these findings indicate that the dietary compound apigenin stabilizes mitochondrial function during inflammation preventing endothelial cell damage and thus provide new translational opportunities for the use of dietary components in the prevention and treatment of inflammatory diseases.

摘要

急性和慢性炎症的特征是活性氧(ROS)产生增加、线粒体代谢失调和免疫功能异常,这导致了心血管疾病和败血症。临床和流行病学研究表明,饮食干预对炎症性疾病可能有潜在的益处,但人们对营养素如何发挥作用的理解仍然不足。在本研究中,我们评估了在炎症过程中,一种在我们饮食中丰富存在的抗炎类黄酮芹菜素对内皮细胞的影响。在这里,我们表明,芹菜素通过降低 ROS 产生和 caspase-3 的活性,减少了脂多糖(LPS)诱导的细胞凋亡。芹菜素对 LPS 诱导的线粒体功能障碍提供了保护,并重新建立了正常的线粒体复合物 I 活性,这是电子泄漏和超氧化物产生的主要部位,表明其在炎症过程中调节内皮细胞代谢功能的能力。总的来说,这些发现表明,膳食化合物芹菜素在炎症过程中稳定了线粒体功能,防止了内皮细胞损伤,从而为饮食成分在预防和治疗炎症性疾病中的应用提供了新的转化机会。

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Apigenin protects endothelial cells from lipopolysaccharide (LPS)-induced inflammation by decreasing caspase-3 activation and modulating mitochondrial function.芹菜素通过降低 caspase-3 激活和调节线粒体功能来保护内皮细胞免受脂多糖 (LPS) 诱导的炎症。
Int J Mol Sci. 2013 Aug 28;14(9):17664-79. doi: 10.3390/ijms140917664.
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Research progress on antisepsis effect of apigenin and its mechanism of action.芹菜素的抗菌作用及其作用机制的研究进展
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Idiopathic pulmonary fibrosis (IPF): disease pathophysiology, targets, and potential therapeutic interventions.特发性肺纤维化(IPF):疾病病理生理学、靶点和潜在的治疗干预措施。
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The Role of Palmitic Acid in the Co-Toxicity of Bacterial Metabolites to Endothelial Cells.棕榈酸在细菌代谢物对血管内皮细胞共毒性中的作用。
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Apigenin attenuates LPS-induced neurotoxicity and cognitive impairment in mice via promoting mitochondrial fusion/mitophagy: role of SIRT3/PINK1/Parkin pathway.芹菜素通过促进线粒体融合/自噬减轻 LPS 诱导的小鼠神经毒性和认知障碍:SIRT3/PINK1/Parkin 通路的作用。
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Apigenin induces DNA damage through the PKCδ-dependent activation of ATM and H2AX causing down-regulation of genes involved in cell cycle control and DNA repair.芹菜素通过依赖蛋白激酶 Cδ(PKCδ)的 ATM 和 H2AX 的激活诱导 DNA 损伤,导致参与细胞周期控制和 DNA 修复的基因下调。
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Endotoxemia impairs heart mitochondrial function by decreasing electron transfer, ATP synthesis and ATP content without affecting membrane potential.内毒素血症通过降低电子传递、ATP 合成和 ATP 含量而损害心肌线粒体功能,而不影响膜电位。
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Flavone deglycosylation increases their anti-inflammatory activity and absorption.黄酮去糖基化增加了它们的抗炎活性和吸收。
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