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嘌呤能外切酶参与克氏锥虫急性感染小鼠的血栓调节。

Purinergic ecto-enzymes participate in the thromboregulation in acute in mice infection by Trypanosoma cruzi.

作者信息

do Carmo Guilherme M, Doleski Pedro H, de Sá Mariângela F, Grando Thirssa H, Bottari Nathieli B, Leal Daniela B R, Gressler Lucas T, Mendes Ricardo E, Stefani Lenita M, Monteiro Silvia G, Da Silva Aleksandro S

机构信息

Department of Biochemistry and Molecular Biology, Universidade Federal de Santa Maria (UFSM), Santa Maria, Brazil.

Department of Microbiology and Parasitology, Universidade Federal de Santa Maria (UFSM), Santa Maria, RS, Brazil.

出版信息

Mol Cell Biochem. 2017 Aug;432(1-2):1-6. doi: 10.1007/s11010-017-2992-2. Epub 2017 Mar 11.

Abstract

Coagulation disorders have been described in Chagas disease with thrombocytopenia as an important event. Several mechanisms may be related to this pathogenesis, such as enzymes of the purinergic system, purine, and receptors involved in the regulation and modulation of physiological events related to hemostasis. Therefore, the aim of this study was to evaluate the activities of E-NTPDase, E-5'nucleotidase, and ecto-adenosine deaminase (E-ADA) in platelets of mice experimentally infected by Trypanosoma cruzi. Twelve female mice were used, divided into two groups (n = 6): uninfected and infected. Mice of infected group were intraperitoneally inoculated with 10 trypomastigotes of T. cruzi (strain Y). On day 12 post-infection (PI), blood samples were collected for quantitation and separation of platelets. A significant reduction in the number of platelets of infected mice (P < 0.05) was observed. The activities of E-NTPDase (ATP and ADP substrates), E-5'nucleotidase, and E-ADA in platelets increased significantly (P < 0.05) in mice infected by T. cruzi compared with uninfected animals. A negative correlation (P < 0.01)was observed between the number of platelets and ATP hydrolysis (r = -0.64), and ADP hydrolysis (r = -0.69) by E-NTPDase. Therefore, there is a response from the purinergic system activating ecto-enzymes in platelets of mice T. cruzi infected, as a compensatory effect of thrombocytopenia.

摘要

在恰加斯病中已描述了凝血障碍,血小板减少是一个重要事件。几种机制可能与这种发病机制有关,例如嘌呤能系统的酶、嘌呤以及参与止血相关生理事件调节的受体。因此,本研究的目的是评估实验感染克氏锥虫的小鼠血小板中E-NTPD酶、E-5'核苷酸酶和胞外腺苷脱氨酶(E-ADA)的活性。使用了12只雌性小鼠,分为两组(n = 6):未感染组和感染组。感染组小鼠腹腔内接种10个克氏锥虫(Y株)的锥鞭毛体。在感染后第12天(PI),采集血样用于血小板的定量和分离。观察到感染小鼠的血小板数量显著减少(P < 0.05)。与未感染动物相比,感染克氏锥虫的小鼠血小板中E-NTPD酶(ATP和ADP底物)、E-5'核苷酸酶和E-ADA的活性显著增加(P < 0.05)。血小板数量与E-NTPD酶对ATP水解(r = -0.64)和ADP水解(r = -0.69)之间存在负相关(P < 0.01)。因此,嘌呤能系统有反应,激活了感染克氏锥虫的小鼠血小板中的胞外酶,作为血小板减少的一种代偿效应。

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