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褪黑素可降低循环负荷,而对组织寄生虫复制无影响。

Melatonin decreases circulating load with no effect on tissue parasite replication.

机构信息

Departamento de Análises Clínicas, Toxicológicas e Bromatológicas, DACTB, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo (USP), Ribeirão Preto, São Paulo, Brazil.

Laboratório de Farmacologia, DEPCH, Escola de Enfermagem de Ribeirão Preto, Universidade de São Paulo (USP), Ribeirão Preto, São Paulo, Brazil.

出版信息

Can J Physiol Pharmacol. 2021 Aug;99(8):795-802. doi: 10.1139/cjpp-2020-0473. Epub 2020 Dec 9.

DOI:10.1139/cjpp-2020-0473
PMID:33296274
Abstract

Cardiac damage during the acute phase of Chagas disease (CD) is associated with an increase in pro-inflammatory markers and oxidative stress. Melatonin (MEL) has emerged as a promising therapy for CD due to its antioxidant and immunomodulatory properties; however, the protective action of MEL in the cardiac tissue, as well as its direct action on the parasite cycle, is not fully understood. We investigated the effects of MEL on heart parasitism in mice infected with and also its effects on the parasitic proliferation in vitro. Our in vivo study showed that MEL reduced circulating parasitemia load, but did not control tissue (heart, liver, and spleen) parasitism in mice. MEL did not prevent the redox imbalance in the left ventricle of infected mice. Our in vitro findings showed that MEL did not inhibit parasites replication within cells, but rather increased their release from cells. MEL did not control parasitism load in the heart or prevent the cardiac redox imbalance induced by acute infection. The hormone controlled the circulating parasitic load, but within cells MEL accelerated parasitic release, a response that can be harmful.

摘要

恰加斯病(CD)急性期的心脏损伤与促炎标志物和氧化应激的增加有关。褪黑素(MEL)因其抗氧化和免疫调节特性而成为治疗 CD 的一种有前途的方法;然而,MEL 在心脏组织中的保护作用及其对寄生虫周期的直接作用尚不完全清楚。我们研究了 MEL 对感染 的小鼠心脏寄生虫感染的影响,以及它对寄生虫体外增殖的影响。我们的体内研究表明,MEL 降低了循环寄生虫载量,但不能控制感染小鼠的组织(心脏、肝脏和脾脏)寄生虫感染。MEL 没有预防感染小鼠左心室的氧化还原失衡。我们的体外研究结果表明,MEL 并没有抑制细胞内寄生虫的复制,而是增加了寄生虫从细胞中的释放。MEL 不能控制心脏中的寄生虫感染负荷,也不能预防急性 感染引起的心脏氧化还原失衡。该激素控制循环寄生虫载量,但在细胞内,MEL 加速寄生虫释放,这种反应可能有害。

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