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长五聚素家族成员 3 在自发性高血压心力衰竭大鼠中的保护作用。

The Protective Role of the Long Pentraxin PTX3 in Spontaneously Hypertensive Rats with Heart Failure.

机构信息

Department of Critical Care Medicine, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.

Department of Gastroenterology, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.

出版信息

Cardiovasc Toxicol. 2021 Oct;21(10):808-819. doi: 10.1007/s12012-021-09671-0. Epub 2021 Jun 25.

Abstract

Pentraxin 3 (PTX3) is synthesized locally and released into the circulation, reflecting local inflammation in the cardiovascular system. Therefore, we conducted a study to explore the effect of PTX3 in spontaneously hypertensive heart failure (SHHF) rats. Sprague Dawley (SD) and SHHF rats were treated with recombinant PTX3 protein, and the blood pressure (BP) and echocardiographic parameters were collected. Radioimmunoassay, enzyme immunoassay and enzyme-linked immunosorbent assay (ELISA) were applied to detect plasma levels of atrial/B-type natriuretic peptide (ANP/BNP) and PTX3. The pathological changes in the myocardial tissues were observed by hematoxylin and eosin (HE) and Masson stainings. The mRNA and protein expressions were detected by quantitative real-time reverse-transcription polymerase chain reaction (qPCR) and western blotting. Cardiomyocyte apoptosis was evaluated by TUNEL staining and DNA fragmentation test. Increased plasma concentrations of PTX3 were found in SHHF rats compared with SD rats, which was further enhanced by recombinant PTX3 protein. After injection with recombinant PTX3 protein, the heart function was improved in SHHF rats with the decreased systolic and diastolic BP, and the reduced plasma levels of ANP and BNP. Moreover, PTX3 improved the myocardial damage and interstitial fibrosis in SHHF rats with reduced cardiomyocyte apoptosis and decreased mRNA expressions of pro-inflammatory factors in myocardial tissues. PTX3 could decrease the BP and plasma levels of ANP and BNP in SHHF rats, as well as improve the inflammation, cardiomyocyte apoptosis, and pathological changes of myocardial tissues, suggesting it may be a useful intervention in the treatment of SHHF.

摘要

血清淀粉样蛋白 P 成分 3(PTX3)在体内局部合成并释放入血,反映心血管系统局部炎症。因此,我们进行了一项研究,以探讨 PTX3 在自发性高血压性心力衰竭(SHHF)大鼠中的作用。给予 Sprague Dawley(SD)大鼠和 SHHF 大鼠重组 PTX3 蛋白,并收集血压(BP)和超声心动图参数。应用放射免疫测定法、酶联免疫吸附测定法和酶联免疫吸附试验(ELISA)检测血浆心房/B 型利钠肽(ANP/BNP)和 PTX3 水平。通过苏木精和伊红(HE)及 Masson 染色观察心肌组织的病理变化。通过实时定量逆转录聚合酶链反应(qPCR)和蛋白质印迹法检测 mRNA 和蛋白表达。通过 TUNEL 染色和 DNA 片段化试验评估心肌细胞凋亡。与 SD 大鼠相比,SHHF 大鼠的血浆 PTX3 浓度升高,重组 PTX3 蛋白进一步增强了这种升高。注射重组 PTX3 蛋白后,SHHF 大鼠的心脏功能得到改善,收缩压和舒张压降低,血浆 ANP 和 BNP 水平降低。此外,PTX3 改善了 SHHF 大鼠的心肌损伤和间质纤维化,减少了心肌细胞凋亡,降低了心肌组织中促炎因子的 mRNA 表达。PTX3 可降低 SHHF 大鼠的 BP 和血浆 ANP 和 BNP 水平,改善炎症、心肌细胞凋亡和心肌组织的病理变化,提示其可能是治疗 SHHF 的一种有用干预手段。

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