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首页> 外文期刊>Scientific Research and Essays >The effect of extracted bacterial LPS from Salmonella enteritidis on COX-2 in hepg2 cell line in induction and inhibition conditions
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The effect of extracted bacterial LPS from Salmonella enteritidis on COX-2 in hepg2 cell line in induction and inhibition conditions

机译:肠炎沙门氏菌提取的细菌LPS在诱导和抑制条件下对hepg2细胞系COX-2的影响

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Hepatocellular carcinoma is the fifth most common neoplasm and the most important cause of death in patients with liver cirrhosis in the world. lipopolysaccharide (LPS) stimulates the hepatocyte cells and increases the production of inducible cytokine with the high production of nitric oxide and ROS. Chronic inflammation caused by lipopolysaccharide directly activates immune system and indirectly, through COX-2 interferes in the formation of malignant disease. In this study, the rate change of COX-2 was searched by adding LPS and also the effect of inhibition of this inflammatory enzyme by Celecoxib and combined effect of this in HepG2 cancer cells was assessed.Salmonellaenteritidis lipopolysaccharide is extracted by methanol-chloroform method and the Sodium dodesyl sulfate poly acryl-amide gel electrophoresis (SDS-PAGE) electrophoresis bands were stained by silver nitrate. Four treatment groups of HepG2 cells were stimulated with 100 ng/ml LPS, 500 µM Celecoxib as inhibitor and were incubated for 12 and 24 h. Variables including both increase and decrease inflammatory factor, COX-2, was assayed. The obtained results showed that initial activity of COX-2 in not stimulated in HepG2 cell, 1.957 ng/ml after stimulation with LPS for 12 and 24 h (1.383 and 0.618 ng/ml) decreased and the effect of this inhibitor was also studied. The data showed that the reduction of COX-2 in HepG2 cells was correlated with the cell density and duration of incubation with LPS. Inhibition of enzyme associated with inflammation, with inhibitor substance; celecoxib, observed as well as LPS. We can potentially design drugs to treat a variety of diseases and cancers.
机译:肝细胞癌是世界上第五大最常见的肿瘤,也是世界肝硬化患者最重要的死亡原因。脂多糖(LPS)可以刺激肝细胞并增加一氧化氮和ROS的产生,从而诱导细胞因子的产生。脂多糖引起的慢性炎症直接激活免疫系统,并通过COX-2间接干扰恶性疾病的形成。本研究通过添加LPS来研究COX-2的速率变化,并评估塞来昔布对该炎症酶的抑制作用,并评估其在HepG2癌细胞中的联合作用。通过甲醇-氯仿法提取沙门氏肠杆菌脂多糖用硝酸银对十二烷基硫酸钠聚丙烯酰胺凝胶电泳(SDS-PAGE)电泳条带进行染色。用100ng / ml LPS,500μMCelecoxib作为抑制剂刺激HepG2细胞的四个处理组,并孵育12和24小时。分析了包括增加和减少的炎症因子COX-2在内的变量。所得结果表明,在LPS刺激12和24小时(1.383和0.618 ng / ml)后,未在HepG2细胞中刺激的COX-2的初始活性(1.953 ng / ml)降低(1.383和0.618 ng / ml),并研究了该抑制剂的作用。数据显示,HepG2细胞中COX-2的减少与细胞密度和LPS孵育时间有关。用抑制剂物质抑制与炎症有关的酶;塞来昔布,以及LPS。我们可以潜在地设计用于治疗各种疾病和癌症的药物。

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