首页> 外文期刊>Pain research & management: the journal of the Canadian Pain Society = journal de la socie?te? canadienne pour le traitement de la douleur >Human Urinary Kallidinogenase Reduces Lipopolysaccharide-Induced Neuroinflammation and Oxidative Stress in BV-2 Cells
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Human Urinary Kallidinogenase Reduces Lipopolysaccharide-Induced Neuroinflammation and Oxidative Stress in BV-2 Cells

机译:人类尿液中的Kallidinogenase减少BV-2细胞中脂多糖诱导的神经炎症和氧化应激。

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Migraine is one of the most common neurological disorders which poses significant socioeconomic burden worldwide. Neuroinflammation and oxidative stress both play important roles in the pathogenesis of migraine. Human urinary kallidinogenase (UK) is a tissue kallikrein derived from human urine. Increasing evidence suggests that UK may protect against ischemic stroke, but UK’s treatment potential against migraine remains to be explored. Immortal BV-2 murine microglial cells were treated with UK (125?nM, 250?nM, and 500?nM) and then given lipopolysaccharides (LPS, 1000?ng/mL). Cell viability of BV-2?cells was tested by the CCK-8 assay. Expressions of tumor necrosis factor-α (TNFα), prostaglandin E2 (PGE2), interleukin-6 (IL-6), and interleukin-1β (IL-1β) were examined with the ELISA method and western blot. Intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) were measured to determine oxidative stress. Our results showed that LPS administration increased the levels of proinflammatory cytokines (TNFα, PGE2, IL-6, and IL-1β) and oxidative stress (ROS and MDA) when compared with the control group and decreased significantly upon introduction with UK. Taken together, UK treatment reduced LPS-induced neuroinflammation and oxidative stress in a dose-dependent manner, which might be a potential treatment of migraine.
机译:偏头痛是最常见的神经系统疾病之一,在世界范围内构成了巨大的社会经济负担。神经炎症和氧化应激均在偏头痛的发病机理中起重要作用。人尿激肽原酶(UK)是一种源自人尿的激肽释放酶。越来越多的证据表明英国可能预防缺血性中风,但英国对偏头痛的治疗潜力仍有待探索。用UK(125?nM,250?nM和500?nM)处理永生的BV-2鼠小胶质细胞,然后给予脂多糖(LPS,1000?ng / mL)。通过CCK-8测定法检测BV-2α细胞的细胞活力。用ELISA法和蛋白质印迹法检测肿瘤坏死因子-α(TNFα),前列腺素E2(PGE2),白介素-6(IL-6)和白介素-1β(IL-1β)的表达。测量细胞内活性氧(ROS)和丙二醛(MDA)以确定氧化应激。我们的结果表明,与对照组相比,LPS给药可增加促炎细胞因子(TNFα,PGE2,IL-6和IL-1β)和氧化应激(ROS和MDA)的水平,并在引入UK后显着降低。综上所述,UK治疗以剂量依赖性方式减少LPS诱导的神经炎症和氧化应激,这可能是偏头痛的潜在治疗方法。

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