Leukotriene B4

白三烯 B4
  • 文章类型: Journal Article
    呼出气冷凝液(EBC)收集是一种非侵入性采样方法,可通过测量炎症介质来提供有关呼吸系统健康状况的有价值的信息。如pH值,过氧化氢,和白三烯B4.此范围审查旨在提供有关马匹中EBC的收集和分析的最新信息。系统检索三个电子数据库,PubMed,谷歌学者,科学直接,确定了40,978篇文章,其中1590个重复被排除。此外,由于与本评论无关,有39,388篇文章被排除在外,比如对其他物种的研究,呼吸呼气的研究,reviews,和论文。最后,我们在这篇综述中评估了14篇文章.我们的审查显示了集合中的显着差异,storage,和处理EBC样品,强调需要标准化技术和使用特定设备来改进结果的解释。
    Exhaled breath condensate (EBC) collection is a non-invasive sampling method that provides valuable information regarding the health status of the respiratory system by measuring inflammatory mediators, such as pH, hydrogen peroxide, and leukotriene B4. This scoping review aimed to provide an update on the collection and analysis of EBC in horses. A systematic search of three electronic databases, PubMed, Google Scholar, Science Direct, identified 40,978 articles, of which 1590 duplicates were excluded. Moreover, 39,388 articles were excluded because of irrelevance to this review, such as studies on other species, studies on respiratory exhalation, reviews, and theses. Finally, we evaluated 14 articles in this review. Our review revealed significant differences in the collection, storage, and processing of EBC samples, emphasizing the need for standardizing the technique and using specific equipment to improve the interpretation of the results.
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  • 文章类型: Review
    除了吸烟,肺癌可能是由其他因素引起的,包括镉等重金属,镍,砷,铍和六价铬[Cr(VI)],在多个设置中使用,导致广泛的环境和职业暴露以及大量使用。Cr(VI)引起肺癌的机制尚不完全清楚。目前,染色体不稳定是Cr(VI)诱导癌症发生机制的关键过程,先前的研究表明,Cr(VI)通过引发组织损伤和炎症而影响小鼠的肺组织。然而,Cr(VI)诱导炎症的机制及其在肺癌中的确切作用尚不清楚。因此,本综述旨在系统回顾以往评估Cr(VI)诱导炎症的研究,并总结Cr(VI)诱导炎症的主要炎症途径。在细胞培养研究中,COX2,VEGF,JAK-STAT,白三烯B4(LTB4),MAPK,NF-κB和Nrf2信号通路被Cr(VI)一致上调,清楚地表明这些途径与Cr(VI)诱导的炎症有关。此外,Akt信号也被证明有助于Cr(VI)诱导的炎症,尽管报告了不同的发现。在动物模型中很少进行机械研究,其中Cr(VI)上调氧化途径,肺组织中NF-kB信号和MAPK通路。类似于细胞培养研究,报告了Cr(VI)对Akt信号的相反作用。这项工作提供了对Cr(VI)诱导肺部炎症的机制的见解。然而,研究设计中的不同发现和其他主要问题,在细胞和动物模型中,提示需要进一步的研究来揭示Cr(VI)诱导的炎症机制及其在肺癌中的作用。
    Besides smoking, lung cancer can be caused by other factors, including heavy metals such as cadmium, nickel, arsenic, beryllium and hexavalent chromium [Cr(VI)], which is used in multiple settings, resulting in widespread environmental and occupational exposures as well as heavy use. The mechanism by which Cr(VI) causes lung cancer is not completely understood. Currently, it is admitted chromosome instability is a key process in the mechanism of Cr(VI)-induced cancer, and previous studies have suggested Cr(VI) impacts the lung tissue in mice by triggering tissue damage and inflammation. However, the mechanism underlying Cr(VI)-induced inflammation and its exact role in lung cancer are unclear. Therefore, this review aimed to systematically examine previous studies assessing Cr(VI)-induced inflammation and to summarize the major inflammatory pathways involved in Cr(VI)-induced inflammation. In cell culture studies, COX2, VEGF, JAK-STAT, leukotriene B4 (LTB4), MAPK, NF-ҡB and Nrf2 signaling pathways were consistently upregulated by Cr(VI), clearly demonstrating that these pathways are involved in Cr(VI)-induced inflammation. In addition, Akt signaling was also shown to contribute to Cr(VI)-induced inflammation, although discrepant findings were reported. Few mechanistic studies were performed in animal models, in which Cr(VI) upregulated oxidative pathways, NF-kB signaling and the MAPK pathway in the lung tissue. Similar to cell culture studies, opposite effects of Cr(VI) on Akt signaling were reported. This work provides insights into the mechanisms by which Cr(VI) induces lung inflammation. However, discrepant findings and other major issues in study design, both in cell and animal models, suggest that further studies are required to unveil the mechanism of Cr(VI)-induced inflammation and its role in lung cancer.
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  • 文章类型: Journal Article
    OBJECTIVE: Rheumatoid arthritis (RA) is a chronic, autoimmune inflammatory disease of multiple joints that puts the patient at high risk for developing cardiovascular diseases (CVDs). The aim of the present study was to conduct an up-to-date systematic review and meta-analysis of published randomized controlled trials (RCTs) to assess potential changes in RA disease activity, inflammation, and CVD risk after oral intake of ω-3 polyunsaturated fatty acids.
    METHODS: Publications up to July 31, 2016 were examined using the PubMed, SCOPUS, and EMBASE databases.
    METHODS: English language; human subjects; both sexes; RCTs; oral intake of ω-3 fatty acids; minimum duration of 3 mo; and no medication change throughout intervention. The Cochrane Risk of Bias tool was used to assess quality of trials. We included 20 RCTs, involving 717 patients with RA in the intervention group and 535 RA patients in the control group.
    RESULTS: Despite the evidence of overall low quality of trials, consumption of ω-3 fatty acids was found to significantly improve eight disease-activity-related markers. Regarding inflammation, only leukotriene B4 was reduced (five trials, standardized mean difference [SMD], -0.440; 95% confidence interval [CI], -0.676 to -0.205; I2 = 46.5%; P < 0.001). A significant amelioration was found for blood triacylglycerol levels (three trials, SMD, -0.316; 95% CI, -0.561 to -0.070; I2 = 0.0%; P = 0.012).
    CONCLUSIONS: The beneficial properties of ω-3 polyunsaturated fatty acids on RA disease activity confirm the results of previous meta-analyses. Among five proinflammatory markers evaluated, only leukotriene B4 was found to be reduced. However, a positive effect on blood lipid profile of patients with RA was evident, perhaps for the first time.
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  • 文章类型: Journal Article
    背景:海洋衍生的n-3多不饱和脂肪酸(PUFA)可能通过降低促炎性类二十烷酸浓度对炎症具有有益作用。我们旨在评估海洋衍生的n-3PUFA对前列腺素E2(PGE2)的影响,血栓烷B2(TXB2),和白三烯B4(LTB4)通过随机对照试验的系统评价和荟萃分析。
    结果:PubMed上的结构化搜索策略,在这项荟萃分析中,进行了截至2015年11月的WebofScience和Cochrane。在随机效应模型中,使用标准平均差来计算海洋衍生的n-3PUFA对PGE2,TXB2和LTB4的效应大小。本系统评价和荟萃分析共纳入18项RCT,共826名受试者。补充海洋来源的n-3PUFA可显着降低心血管疾病高风险受试者(SMD:-1.26;95%CI:-1.65,-0.86)和不健康受试者(患有非慢性自身免疫性疾病或自身免疫性疾病的受试者)中性粒细胞中LTB4的血清/血浆中TXB2的浓度(SMD:-0.59:95%CI:-1.02,-0.16)。亚组分析显示,类风湿关节炎患者的LTB4显着降低(SMD:-0.83;95%CI:-1.37,-0.29),但在非自身免疫性慢性病患者中没有(SMD:-0.33;95%CI:-0.97,0.31)。在荟萃分析中没有发现显著的发表偏倚。
    结论:海洋衍生的n-3PUFA对降低CVD高风险受试者血液中TXB2的浓度以及不健康受试者中性粒细胞中LTB4具有有益作用,并且患有RA的受试者在补充海洋来源的n-3PUFA的情况下显示较低的LTB4含量。
    BACKGROUND: Marine-derived n-3 polyunsaturated fatty acids (PUFA) may have a beneficial effect on inflammation via lowering pro-inflammatory eicosanoid concentrations. We aimed to assess the effect of marine-derived n-3 PUFA on prostaglandin E2 (PGE2), thromboxane B2 (TXB2), and leukotriene B4 (LTB4) through systematic review and meta-analysis of randomized controlled trials.
    RESULTS: A structured search strategy on PubMed, Web of Science and Cochrane up to November 2015 was undertaken in this meta-analysis. Standard mean difference was used to calculate the effect size of marine-derived n-3 PUFA on PGE2, TXB2 and LTB4 in a random-effect model. A total of 18 RCTs with 826 subjects were included in this systematic review and meta-analysis. Supplementation of marine-derived n-3 PUFA significantly decreased concentrations of TXB2 in serum/plasma in subjects with high risk of cardiovascular diseases (SMD:-1.26; 95% CI: -1.65, -0.86) and LTB4 in neutrophils in unhealthy subjects (subjects with non-autoimmune chronic diseases or auto-immune diseases) (SMD:-0.59: 95% CI: -1.02, -0.16). Subgroup analyses showed a significant reduction of LTB4 in subjects with rheumatoid arthritis (SMD: -0.83; 95% CI: -1.37, -0.29), but not in non-autoimmune chronic disease patients (SMD: -0.33; 95% CI: -0.97, 0.31). No significant publication bias was shown in the meta-analysis.
    CONCLUSIONS: Marine-derived n-3 PUFA had a beneficial effect on reducing the concentration of TXB2 in blood of subjects with high risk of CVD as well as LTB4 in neutrophils in unhealthy subjects, and that subjects with RA showed lower LTB4 content with supplementation of marine-derived n-3 PUFA.
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  • 文章类型: Editorial
    The etiology of inflammatory bowel disease (IBD) is not yet known, but many factors such as defects in the immune system, oxidative stress, microbial content in the gastrointestinal tract, nuclear factor (NF)-κB, nitric oxide (NO), cyclooxygenase-2 (Cox-2), and leukotriene B4 (LB4) are thought to play a role in its pathogenesis. In traditional Iranian medicine (TIM), several medicinal plants are thought to be effective for the treatment of IBD. In this study, information on all of these remedies were derived from all available old sources such as documents or notes and books and were added to the information derived from modern medical databases covering all in vitro, in vivo and clinical trials. For some of these plants, only one or two mechanisms of action have been found such as in Cassia fistula, Lepidium sativum, and Bunium persicum. However, for some plants various mechanisms of action are known. For example, Commiphora mukul is effective in IBD due to its immunomodulatory, antioxidant, and antibacterial properties and it decreases NF-κB, NO and Cox-2. Another herb, Plantago ovata, has immunomodulatory, antioxidant, anti-inflammatory and wound healing activities and decreases NO and LB4. Considering the mechanisms of action of these plants, the combination of some of them may be useful because of their many mechanisms of action such as Pistacia lentiscus, Bunium persicum, Solanum nigrum, Plantago ovata, Boswellia, Solanum nigrum, Plantago ovata and Commiphora mukul. For some of the herbal products used in TIM such as oleogum resin from Commiphora myrrha, seeds of Ocimum basilicum, seeds of Linum usitatissimum, gum resin of Dracaena cinnabari, seeds of Plantago major, seeds of Lallementia royleana, and seeds of Allium porrum, there is no or not enough studies to confirm their benefits in IBD. It is suggested that an evaluation of the effects of these plants on different aspects of IBD should be performed.
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  • 文章类型: Journal Article
    Because of potential adverse events and lack of effectiveness of standard therapies, the use of complementary and alternative medicines (CAM), particularly of herbal therapies, for inflammatory bowel disease (IBD) is increasing. Results from the use of herbal therapies for managing IBD are promising, and no serious adverse events have been reported from them. Herbal therapies show their benefit in managing IBD by different mechanisms such as immune system regulation, antioxidant activity, inhibition of leukotriene B4, inhibition of nuclear factor-kappa B (NF-kappaB), and antiplatelet activity. In this paper, all reported herbal therapies established in animal IBD models or used for managing human IBD are systematically reviewed and their possible mechanisms of action discussed. Conducting clinical trials with high quality and validity (randomized, double blinded, controlled, on a large number of patients) to obtain more conclusive results about the use of herbal therapies in IBD is recommended.
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  • 文章类型: Journal Article
    收集呼出气(EB)和呼出气冷凝液(EBC)是从下气道获得样品的非侵入性方法。虽然这种技术已经很好地用于人类医学中的下呼吸道疾病的诊断,在兽医学中只有少数研究。本文批判性地回顾了迄今为止发表的各种动物物种的收集方法和测量的参数值,并指出了进一步研究的方向。
    Collection of exhaled breath (EB) and exhaled breath condensate (EBC) is a noninvasive method for obtaining samples from the lower airways. While this technique has been well established for the diagnosis of lower respiratory tract diseases in human medicine, only a few studies have been performed in veterinary medicine. This article critically reviews the collection methods and parameter values measured in various animal species published to date and points out directions for further research.
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  • 文章类型: Comparative Study
    白三烯(LTs)C4,D4和E4,过敏反应慢反应物质(SRS-A)的公认成分,先前已显示对豚鼠肺和回肠平滑肌具有收缩活性;LTB4已显示在体外对嗜中性粒细胞具有趋化活性。根据通过使用SRS-ALTs和LTB4的结构类似物获得的数据,我们最近确定了每个部分生物学功能的许多结构基础。关于SRS-A白三烯,类似物在肽侧链和/或羟基的位置与天然结构不同,烯键的数量和位置,光学活动中心的手性,或C-1至C-6区域中的四个极性取代基的结构。LTB4的类似物,其烯键的立体化学不同,在体外评估趋化活性,利用人类嗜中性粒细胞,并在恒河猴体内皮内。我们建议,对于SRS-ALTs,豚鼠的肺实质上存在真正的受体,对于LTB4,灵长类中性粒细胞上存在真正的受体。Further,LTC4,LTD4和LTE4已被证明会在人类皮肤中引起风团和长时间的耀斑,而LTB4唤起了时间依赖性的硬结。这些次要介质的相互作用对于完全发展的宿主对免疫和非免疫损伤的炎症反应可能是关键的。
    Leukotrienes (LTs) C4, D4 and E4, the recognized components of slow reacting substance of anaphylaxis (SRS-A), have previously been shown to have contractile activities for guinea pig pulmonary and ileal smooth muscles; LTB4 has been shown to possess chemotactic activity for neutrophils in vitro. Based on data obtained by the use of structural analogs of the SRS-A LTs and of LTB4, we have recently determined a number of the structural bases for the biological function of each moiety. With regard to the SRS-A leukotrienes, analogs differed from the native structures in the position of the peptide side chain and/or the hydroxyl group, the number and position of ethylenic bonds, the chirality at optically-active centers, or the structures of the four polar substituents in the C-1 to C-6 region. Analogs of LTB4, differing in the stereochemistry of their ethylenic bonds, were evaluated for chemotactic activity both in vitro, using human neutrophils, and in vivo intracutaneously in the rhesus monkey. We propose that true receptors exist on the pulmonary parenchyma of the guinea pig for the SRS-A LTs and on the primate neutrophil for LTB4. Further, LTC4, LTD4 and LTE4 have been shown to elicit a wheal and prolonged flare in human skin, whereas LTB4 evokes a time-dependent induration. The interaction of these secondary mediators may be critical to a fully developed host inflammatory response to both immunologic and non-immunologic injury.
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