首页> 外文会议>Biomedical Engineering and Biotechnology (iCBEB), 2012 International Conference on >Lily Polysaccharide Prevents Alloxan-induced HIT-T15 Cell Damage by Reducing ROS Generation
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Lily Polysaccharide Prevents Alloxan-induced HIT-T15 Cell Damage by Reducing ROS Generation

机译:百合多糖通过减少ROS的生成来防止四氧嘧啶诱导的HIT-T15细胞损伤

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The previous studies of our team and other researchers have shown that two polysaccharides derived from bulbs of lily aqueous extracts (LP-1, LP-2) can decrease fasting blood glucose concentration in diabetic model animal (in vivo). In the present study, we investigated the effects of LP-1 or LP-2 on cultured pancreatic d-cell tumor-derived cell line HIT-T15 that had undergone oxidative damage. The cell viability, insulin secretion, and intracellular reactive oxygen species (ROS) level were investigated in HIT-T15 cells after LP-, alloxan-, or both-treatment, respectively. The metabolic activity of d-cells was determined by MTT assay while the insulin secretion was detected by ELISA technique. Intracellular ROS was detected by fluorescent spectrophotometry using DCFH-DA. The treatment with LP-1 (> 0.5 mg/ml) or LP-2 (> 0.1 mg/ml) could significantly elevated the cell viability compared to untreated normal cells (p 1 mg/ml). Importantly, the viability of cells treated with 10 mg/ml LP-2 were almost restored to the levels of alloxan-untreated cells and completely prevented the lowering of glucose-stimulated insulin release. Our investigation suggested that LP-1 or LP-2 reduced the damage of alloxan-induced HIT-T15 cells through scavenging intracellular ROS level. And these data also provide some information when LP-1 or LP-2 is used as a bioactive component for developing a new anti-diabetic agent.
机译:我们团队和其他研究人员的先前研究表明,两种来自百合水提取物鳞茎的多糖(LP-1,LP-2)可以降低糖尿病模型动物(体内)的空腹血糖浓度。在本研究中,我们调查了LP-1或LP-2对培养的胰腺d细胞肿瘤衍生的细胞系HIT-T15遭受氧化损伤的影响。分别在LP-,四氧嘧啶或两者处理后,在HIT-T15细胞中研究了细胞活力,胰岛素分泌和细胞内活性氧(ROS)水平。 MTT法测定d细胞的代谢活性,ELISA法检测胰岛素分泌。使用DCFH-DA通过荧光分光光度法检测细胞内ROS。与未经处理的正常细胞(p 1 mg / ml)相比,用LP-1(> 0.5 mg / ml)或LP-2(> 0.1 mg / ml)处理可以显着提高细胞活力。重要的是,用10 mg / ml LP-2处理的细胞的活力几乎恢复到未经四氧嘧啶处理的细胞水平,并完全阻止了葡萄糖刺激的胰岛素释放的降低。我们的研究表明LP-1或LP-2通过清除细胞内ROS水平来减少四氧嘧啶诱导的HIT-T15细胞的损伤。当LP-1或LP-2用作开发新型抗糖尿病药的生物活性成分时,这些数据也提供了一些信息。

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