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替格瑞洛对脓毒症诱导的急性肾损伤小鼠模型肾功能的保护作用。

The protective effect of ticagrelor on renal function in a mouse model of sepsis-induced acute kidney injury.

机构信息

a Emergency Center, Shanghai East Hospital , Tongji University School of Medicine , Shanghai , China.

b Intensive Care Unit , Shanghai University of Medicine& Health Sciences Affiliated Zhoupu Hospital , Shanghai , China.

出版信息

Platelets. 2019;30(2):199-205. doi: 10.1080/09537104.2017.1392499. Epub 2018 Jan 25.

DOI:10.1080/09537104.2017.1392499
PMID:29370574
Abstract

Platelets are traditionally considered to be essential components of primary hemostasis. Recent investigations have revealed that platelets can be activated in patients with sepsis and are implicated in the development of sepsis and sepsis-induced-acute kidney injury (SAKI). In the present study, ticagrelor was used to induce a mouse model of SAKI by cecal ligation and puncture. It was found that ticagrelor could inhibit platelet activity, decrease the levels of interleukin-1β and serum creatinine, reduce infiltration of neutrophils in renal tissue, and attenuate cell apoptosis in the kidney. The results suggested that ticagrelor could protect renal function by inhibiting inflammation, recruitment of neutrophils into the kidney, and cell apoptosis in renal tissue. Thus, the findings might provide new strategies for preventing SAKI.

摘要

血小板传统上被认为是初级止血的重要组成部分。最近的研究表明,血小板在脓毒症患者中可以被激活,并与脓毒症和脓毒症引起的急性肾损伤(SAKI)的发展有关。在本研究中,通过盲肠结扎和穿刺诱导替格瑞洛诱导 SAKI 小鼠模型。结果发现,替格瑞洛可以抑制血小板活性,降低白细胞介素-1β和血清肌酐的水平,减少中性粒细胞在肾组织中的浸润,并减轻肾脏细胞凋亡。结果表明,替格瑞洛通过抑制炎症、中性粒细胞向肾脏的募集和肾组织细胞凋亡来保护肾功能。因此,这些发现可能为预防 SAKI 提供新的策略。

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