在Taenia multiceps感染动物中,ADAMTS-13和HMGB1诱导的氧化应激
Gungor Cagdas Dincel1, Orhan Yavuz2, Serkan Yildirim3
1Eskil Vocational School, Laboratory and Veterinary Science, Aksaray University, Aksaray, Turkey. gcdincel@yahoo.com.tr.
Scientific reports
|October 20, 2023
概括
高流动性组盒子1 (HMGB1) 和氧化应激驱动coenurosis中的大脑损伤. 亚当斯-13 (A 解体和金属蛋白酶与血栓胺基因) 可能会保护血脑屏障,为Taenia multiceps感染提供新的治疗点.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 寄生虫学的寄生虫学
背景情况:
- 由Taenia multiceps (影响中枢神经系统) 引起的病.
- 氧化应激 (OS) 及其在神经病理学中的作用
- 在神经疾病中,高流动性组盒1 (HMGB1) 和ADAMTS (A分解蛋白和具有血栓胺基因的金属蛋白酶)
研究的目的:
- 研究coenurosis的神经病变发生的原因.
- 阐明OS,HMGB1和ADAMTS在T. multiceps感染中的作用.
- 确定潜在的生物标志物和治疗点.
主要方法:
- 量化ADAMTS-13,HMGB1,谷氨减少酶 (GR),铜/超氧化物转化酶 (Cu/Zn SOD) 和8-基-2'-脱氧氨酸 (8-OHdG) 的表达.
- 感染和对照动物组之间的比较.
- 分析神经元,内皮细胞和质细胞中的蛋白质表达.
主要成果:
- 在受感染的动物中,ADAMTS-13,HMGB1,GR,Cu/Zn SOD和8-OHdG的水平明显升高.
- HMGB1上调直接与大脑辅酶体破坏相关.
- 增加的ADAMTS-13水平表明在血脑屏障保护中的作用.
- 证据表明HMGB1和ADAMTS-13在微血栓形成中的竞争.
- 首次证明HMGB1和ADAMTS-13表达在coenurosis中的反应性细胞中.
结论:
- 在coenurosis神经病变发生过程中,HMGB1介导的氧化压力至关重要.
- ADAMTS-13在神经保护和血脑屏障完整性方面发挥着作用.
- HMGB1和ADAMTS-13是疾病风险和神经病变的潜在生物标志物.
- HMGB1和ADAMTS-13代表了对毛病的新型治疗点.
- 这项研究强调了涉及HMGB1和ADAMTS-13的神经免疫病理学.
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