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富血小板血浆通过减少 NF-κB 和增强 VEGF 表达发挥抗炎作用,并减轻异丙肾上腺素诱导的心肌毒性模型中心肌细胞损伤。

Platelet-rich plasma exhibits anti-inflammatory effect and attenuates cardiomyocyte damage by reducing NF-κB and enhancing VEGF expression in isoproterenol induced cardiotoxicity model.

机构信息

Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India.

Chitkara College of Pharmacy, Chitkara University, Punjab, India.

出版信息

Environ Toxicol. 2022 Apr;37(4):936-953. doi: 10.1002/tox.23456. Epub 2022 Jan 11.

Abstract

The present study investigated the cardioprotective effects of activated platelet-rich plasma (PRP) on high dose isoproterenol (ISO) induced cardiotoxicity. ISO was injected at a dose of 85 mg/kg/day, s.c. for 2 days. Cardiac function parameters including dp/dt max/min, left ventricular end diastolic pressure (LVEDP), relaxation constant (tau) and electrocardiogram (ECG) changes, anti-oxidant and membrane bound enzymes assays, pro-inflammatory cytokine levels, collagen content, immunohistochemical staining/gene expression of vascular endothelial growth factor (VEGF), cTnI (cardiac troponin I), NF-κB (nuclear factor kappa B), Smad-2/3, TGF-β (transforming growth factor), collagen-1/3 proteins were evaluated. PRP and platelet-poor plasma (PPP) were injected intramyocardially (200 μl in each ventricle region) 3 h after first dose of ISO under anesthesia. ISO injection induced cardiac dysfunction, hypertrophy, fibrosis, necrosis due to decline in anti-oxidant capacity, enhanced NF-κB and reduced cTnI immunostaining. However, the PRP injection attenuated these cardiac pathological changes by exerting anti-inflammatory properties and promoting cardiomyocyte repair.

摘要

本研究探讨了激活血小板富血浆(PRP)对高剂量异丙肾上腺素(ISO)诱导的心脏毒性的心脏保护作用。ISO 以 85mg/kg/天的剂量皮下注射,连续 2 天。评估了心脏功能参数,包括 dp/dt max/min、左心室舒张末期压(LVEDP)、松弛常数(tau)和心电图(ECG)变化、抗氧化和膜结合酶测定、促炎细胞因子水平、胶原含量、血管内皮生长因子(VEGF)、cTnI(心肌肌钙蛋白 I)、NF-κB(核因子 kappa B)、Smad-2/3、TGF-β(转化生长因子)、胶原-1/3 蛋白的免疫组织化学染色/基因表达。PRP 和血小板少血浆(PPP)在 ISO 第一次注射后 3 小时在麻醉下心肌内注射(每个心室区域 200μl)。ISO 注射引起心脏功能障碍、肥大、纤维化和坏死,这是由于抗氧化能力下降、NF-κB 增强和 cTnI 免疫染色减少所致。然而,PRP 注射通过发挥抗炎特性和促进心肌细胞修复来减轻这些心脏病理变化。

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