儿科性综合征:氧化应激和炎症的相互作用
Simachew Yonas Mulat1, Marija Mihajlović1, Tamara Antonić1
1University of Belgrade, Faculty of Pharmacy, Department of Medical Biochemistry, Belgrade.
Journal of medical biochemistry
|August 14, 2024
概括
高血压影响了儿科性综合征中的氧化应激. 较低的抗氧化能力和较高的Pentraxin 3 (PTX3) 表明疾病活性,表明炎症和氧化应激之间的联系.
科学领域:
- 儿科脏病学 儿科脏病学
- 生物化学 生物化学
- 免疫学 免疫学 免疫学
背景情况:
- 导致儿科性综合征 (NS) 的确切机制尚不清楚.
- 这项研究调查了高血压,氧化应激和炎症在急性期NS儿童的相互作用.
研究的目的:
- 探索儿童性综合征中高血压和氧化应激标志物之间的关系.
- 评估炎症和氧化应激在儿科性综合征急性阶段的作用.
主要方法:
- 分析了急性和缓解阶段NS的33名儿童 (2-9岁) 的血清样本.
- 测量了氧化应激标志物 (TOS,AOPP,PAB,-SH,PON1,TAS) 和炎症标志物 (PTX3,莱普丁,PD-L1,E-cadherin) 的测量.
主要成果:
- 在儿科NS患者中,高血压与更高的先进氧化蛋白产物 (AOPP) 和总抗氧化状态 (TAS) 相相关.
- 与缓解相比,急性阶段NS显示硫基 (-SH) 和偏氧酶1 (PON1) 活性下降,Pentraxin 3 (PTX3) 增加和瘦素减少.
- 在急性阶段,PTX3与AOPP和TAS相关,而AOPP与勒呈负相关性.
结论:
- 高血压显著影响了儿科性综合征中的氧化应激.
- 减少的抗氧化能力和升高的PTX3表明在疾病的发病和活动中发挥了作用.
- 莱普也可能参与儿科性综合征内的氧化应激机制.
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