Derangement in Homeostasis of Neutrophil Elastase and its Inhibitory Systems in Ischemic Stroke Patients

Q3 Pharmacology, Toxicology and Pharmaceutics

Biomedical and Pharmacology Journal Pub Date : 2023-06-30 DOI:10.13005/bpj/2669

Mamatha Kunder, A. Kutty, V. Lakshmaiah

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Abstract

Neutrophils are the first to infiltrate ischemic brain regions causing the release of Neutrophil Elastase (NE), a pro-inflammatory proteinase. The activity of NE is well regulated by endogenous inhibitors alpha1-antitrypsin (α1-AT) and alpha2-macroglobulin (α2-MG). The physiological balance of elastase and anti-elastase factors is essential to maintain the normal integrity of tissues and an imbalance has been implicated in the pathogenesis of several acute and chronic inflammatory diseases. The present study was designed to determine the plasma levels of NE, α1-AT, α2-MG, and NE–α1-AT complex to evaluate their role in inflammatory processes of ischemic stroke. The effect of homocysteine on the release of elastase from neutrophils was also studied. The study involved a total of 100 subjects (controls =60 and patients=40). Significantly higher mean elastase activity and lower α1-AT levels were observed in ischemic stroke patients than in controls. NE- α1-AT complex and α2-MG levels were significantly increased in the patient group. The in vitro study indicated homocysteine induced release of elastase from neutrophils. In conclusion, homeostasis of NE and its endogenous inhibitors is deranged in patients suggestive of their role in the pathogenesis of ischemic stroke through exacerbating inflammatory and coagulation processes.

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缺血性脑卒中患者中性粒细胞弹性酶动态平衡紊乱及其抑制系统

中性粒细胞首先渗透到缺血脑区域，引起中性粒细胞弹性酶(NE)的释放，这是一种促炎蛋白酶。NE的活性受内源性抑制剂α1-抗胰蛋白酶(α1-AT)和α2-巨球蛋白(α2-MG)的调控。弹性蛋白酶和抗弹性蛋白酶因子的生理平衡对于维持组织的正常完整性至关重要，并且在一些急慢性炎症性疾病的发病机制中涉及不平衡。本研究旨在测定血浆NE、α1-AT、α2-MG和NE -α1-AT复合物的水平，以评估其在缺血性卒中炎症过程中的作用。还研究了同型半胱氨酸对中性粒细胞释放弹性蛋白酶的影响。该研究共涉及100名受试者(对照组=60，患者=40)。缺血性脑卒中患者的平均弹性酶活性明显高于对照组，α1-AT水平明显低于对照组。患者组NE- α1-AT复合物及α2-MG水平明显升高。体外研究表明，同型半胱氨酸诱导中性粒细胞释放弹性蛋白酶。总之，NE及其内源性抑制剂在患者体内的稳态紊乱，提示它们通过加剧炎症和凝血过程在缺血性卒中发病机制中的作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Biomedical and Pharmacology Journal Pharmacology, Toxicology and Pharmaceutics-Pharmacology

CiteScore

1.20

自引率

0.00%

发文量

189

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