在Trypanosoma cruzi感染的急性阶段,TNF-α部分调节内皮功能障碍
Thales M H Dourado1,2, Wanessa M C Awata1,2, Gustavo F Pimenta1,2
1Programa de Pós-Graduação em Farmacologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo (USP), Ribeirão Preto, Brazil.
British journal of pharmacology
|December 28, 2025
概括
急性Trypanosoma cruzi感染通过增加TNF-α引起血管功能障碍,导致内皮功能障碍和超收缩性. 这项研究揭示了TNF-α作为急性查加斯病血管并发症的关键调解者.
科学领域:
- 心血管研究研究心血管研究
- 传染性疾病 传染性疾病
- 血管生物学 血管生物学
背景情况:
- 以心脏影响而闻名的Trypanosoma cruzi (T. cruzi) 感染对血管系统的影响尚未得到充分研究.
- 在急性和慢性T. cruzi感染期间调查血管反应对于了解疾病病理学至关重要.
研究的目的:
- 为了研究急性和慢性T. cruzi感染对血管反应能力的影响.
- 为了阐明T. cruzi诱导的血管功能障碍的潜在机制.
主要方法:
- 雄性Wistar大鼠感染了T. cruzi (Y菌株) 的病毒.
- 胸前大动脉的血管功能在急性 (9dpi) 和慢性 (60dpi) 感染阶段被评估.
- 使用etanercept进行了瘤亡因子-α (TNF-α) 抑制.
主要成果:
- 急性T. cruzi感染诱导了内皮功能障碍和血管超收缩性.
- 在慢性感染期间没有观察到血管反应的变化.
- 抑制TNF-α可以防止内皮功能障碍,氧化应激 (NOX2/超氧化物生成) 和增加血栓素A2 (TXA2).
结论:
- 瘤亡因子-α (TNF-α) 在T. cruzi感染的急性阶段调解血管功能障碍.
- TNF-α通过超氧化物生成,NOX2上调和增加TXA2产生促进内皮功能障碍和超收缩性.
- 周血管脂肪组织 (PVAT) 显示骨髓氧化酶活性增加,这表明它在中性粒细胞封存中发挥了作用.
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