...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Thrombosis and Haemostasis: Journal of the International Society on Thrombosis and Haemostasis >Oxidative stress and thromboxane-dependent platelet activation in inflammatory bowel disease: effects of anti-TNF-alpha treatment
【24h】

Oxidative stress and thromboxane-dependent platelet activation in inflammatory bowel disease: effects of anti-TNF-alpha treatment

机译：炎性肠病中的氧化应激和血栓烷依赖性血小板活化：抗TNF-α治疗的影响

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Patients with inflammatory bowel disease (IBD) are at higher risk of venous thromboembolism and coronary artery disease despite having a lower burden of traditional risk factors. Platelets from IBD patients release more soluble CD40 ligand (CD40L), and this has been implicated in IBD platelet hyper-activation. We here measured the urinary F-2-isoprostane 8-iso-prostaglandin (PG)(2 alpha) (8-iso-PGF(2 alpha)), urinary 11-dehydro-thronnboxane (TX) B-2 (11-dehydro-TXB2) and plasma CD40L in IBD patients, and explored the in vitro action of anti-tumour necrosis factor (TNF)-alpha antibody infliximab on IBD differentiating megakaryocytes. Urinary and blood samples were collected from 124 IBD patients and 37 healthy subjects. Thirteen IBD patients were also evaluated before and after 6 week infliximab treatment. The in vitro effect of infliximab on patient-derived megakaryocytes was evaluated by immunoflorescence microscopy and by flow cytometry. IBD patients had significantly (p<0.0001) higher urinary 8-iso-PGF(2 alpha) and 11-dehydro-TXB2 as well as plasma CD40L levels than controls, with active IBD patients displaying higher urinary and plasma values when compared to inactive patients in remission. A 6-week treatment with infliximab was associated with a significant reduction of the urinary excretion of 8-iso-PGF2 alpha and 11-dehydro-TXB2 (p=0.008) and plasma CD40L (p=0.001). Infliximab induced significantly rescued pro-platelet formation by megakaryocytes derived from IBD patients but not from healthy controls. Our findings provide evidence for enhanced in vivo TX dependent platelet activation and lipid peroxidation in IBD patients. Anti-TNF-alpha therapy with infliximab down-regulates in vivo isoprostane generation and TX biosynthesis in responder IBD patients. Further studies are needed to clarify the implication of infliximab induced-proplatelet formation from IBD megakaryocytes.
机译：炎症性肠病（IBD）患者的静脉血栓栓塞和冠状动脉疾病的风险较高，尽管传统风险因素的负担较低。 IBD患者的血小板释放出更多的可溶性CD40配体（CD40L），这与IBD血小板的过度活化有关。我们在这里测量了尿中的F-2-异前列腺素8-异前列腺素（PG）（2 alpha）（8-iso-PGF（2 alpha）），尿中的11-脱氢-thronnboxane（TX）B-2（11-脱氢-TXB2）和IBD患者的血浆CD40L，并探讨了抗肿瘤坏死因子（TNF）-α抗体英夫利昔单抗对IBD分化巨核细胞的体外作用。从124名IBD患者和37名健康受试者中采集尿液和血液样本。在6周英夫利昔单抗治疗前后，还评估了13名IBD患者。通过免疫荧光显微镜和流式细胞术评估英夫利昔单抗对患者来源的巨核细胞的体外作用。 IBD患者的尿8-iso-PGF（2 alpha）和11-dehydro-TXB2以及血浆CD40L水平明显高于对照组（p <0.0001），与不活动的患者相比，活跃的IBD患者的尿和血浆值更高在缓解。英夫利昔单抗治疗6周与显着减少8-异-PGF2α和11-脱氢-TXB2（p = 0.008）和血浆CD40L（p = 0.001）的尿排泄相关。英夫利昔单抗诱导的IBD患者而非健康对照组的巨核细胞显着拯救了血小板形成。我们的发现为IBD患者体内TX依赖性血小板活化和脂质过氧化作用增强提供了证据。英夫利昔单抗的抗TNF-α治疗可降低应答性IBD患者的体内异前列腺素生成和TX生物合成。需要进一步的研究来阐明英夫利昔单抗诱导的IBD巨核细胞血小板形成的意义。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号