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番茄红素抑制雨蛙肽刺激的胰腺腺泡细胞中白细胞介素-6 的表达。

Lycopene inhibits IL-6 expression in cerulein-stimulated pancreatic acinar cells.

机构信息

Department of Food and Nutrition, Brain Korea 21 Project, College of Human Ecology, Yonsei University, Seoul, 120-749, Korea.

出版信息

Genes Nutr. 2011 May;6(2):117-23. doi: 10.1007/s12263-010-0195-5. Epub 2010 Dec 5.

DOI:10.1007/s12263-010-0195-5
PMID:21484151
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3092906/
Abstract

Reactive oxygen species (ROS) are known to be involved in the pathogenesis of acute and chronic pancreatitis. The cholecystokinin (CCK) analog cerulein causes pathophysiological, morphological, and biochemical events similar to those observed in human acute pancreatitis. The oxidant-sensitive transcription factor NF-κB plays a critical role in the development of cerulein pancreatitis by regulating the expression of pro-inflammatory cytokines in the pancreas. Lycopene has an anti-oxidant effect in various cells. In the present study, we investigated whether cerulein induces NF-κB activation and IL-6 expression in pancreatic acinar cells and whether lycopene inhibits these events. NF-κB-DNA-binding activity was determined by electrophoretic mobility shift assay, and mRNA expression was analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and real-time RT-PCR analyses. The IL-6 concentration in the medium was determined by enzyme-linked immunosorbent assay. Our results showed that cerulein induced IL-6 expression in a time-dependent manner. NF-κB-DNA-binding activity and intracellular levels of ROS in pancreatic acinar cells were increased by cerulein. Lycopene inhibited the cerulein-induced increase in intracellular ROS, NF-κB activation, and IL-6 expression in pancreatic acinar cells in a dose-dependent manner. In conclusion, lycopene may be beneficial in the prevention and/or treatment of acute pancreatitis by inhibiting the activation of NF-κB and the expression of inflammatory cytokines through reduction in intracellular levels of ROS in pancreatic acinar cells.

摘要

活性氧(ROS)已知参与急性和慢性胰腺炎的发病机制。胆囊收缩素(CCK)类似物蛙皮素引起类似于人类急性胰腺炎的病理生理、形态和生化事件。氧化敏感转录因子 NF-κB 通过调节胰腺中促炎细胞因子的表达,在蛙皮素胰腺炎的发生发展中起关键作用。番茄红素在各种细胞中具有抗氧化作用。在本研究中,我们研究了蛙皮素是否诱导胰腺腺泡细胞中 NF-κB 的激活和 IL-6 的表达,以及番茄红素是否抑制这些事件。通过电泳迁移率变动分析测定 NF-κB-DNA 结合活性,通过逆转录-聚合酶链反应(RT-PCR)和实时 RT-PCR 分析分析 mRNA 表达。通过酶联免疫吸附试验测定培养基中 IL-6 的浓度。我们的结果表明,蛙皮素以时间依赖性方式诱导 IL-6 的表达。NF-κB-DNA 结合活性和胰腺腺泡细胞内 ROS 的水平增加了蛙皮素。番茄红素以剂量依赖性方式抑制胰腺腺泡细胞中 ROS 、 NF-κB 激活和 IL-6 表达的增加。总之,番茄红素可能通过降低胰腺腺泡细胞内 ROS 的水平,抑制 NF-κB 的激活和炎症细胞因子的表达,对急性胰腺炎的预防和/或治疗有益。

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Lycopene suppresses LPS-induced NO and IL-6 production by inhibiting the activation of ERK, p38MAPK, and NF-kappaB in macrophages.番茄红素通过抑制巨噬细胞中 ERK、p38MAPK 和 NF-κB 的激活来抑制 LPS 诱导的 NO 和 IL-6 的产生。
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Rosiglitazone, a peroxisome proliferator-activated receptor gamma (PPARgamma)-specific agonist, as a modulator in experimental acute pancreatitis.罗格列酮,一种过氧化物酶体增殖物激活受体γ(PPARγ)特异性激动剂,作为实验性急性胰腺炎的调节剂。
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Pioglitazone, a PPARgamma ligand, suppresses NFkappaB activation through inhibition of IkappaB kinase activation in cerulein-treated AR42J cells.吡格列酮,一种过氧化物酶体增殖物激活受体γ(PPARγ)配体,通过抑制雨蛙肽处理的AR42J细胞中IκB激酶的激活来抑制核因子κB(NFκB)的激活。
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Effect of lycopene and beta-carotene on peroxynitrite-mediated cellular modifications.番茄红素和β-胡萝卜素对过氧亚硝酸盐介导的细胞修饰的影响。
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The effect of lycopene on cell growth and oxidative DNA damage of Hep3B human hepatoma cells.番茄红素对Hep3B人肝癌细胞的细胞生长及氧化性DNA损伤的影响。
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