Fahmi Alaa N A, Shehatou George S G, Shebl Abdelhadi M, Salem Hatem A
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Mansoura University, Mansoura, 35516, Egypt.
Department of Pathology, Faculty of Medicine, Mansoura University, Mansoura, Egypt.
Naunyn Schmiedebergs Arch Pharmacol. 2016 Mar;389(3):269-78. doi: 10.1007/s00210-015-1202-6. Epub 2015 Dec 28.
The aim of the present work was to investigate possible protective effects of febuxostat, a highly potent xanthine oxidase inhibitor, against acute lung injury (ALI) induced by lipopolysaccharide (LPS) in rats. Male Sprague Dawley rats were randomly divided into six groups, as follows: (i) vehicle control group; (ii) and (iii) febuxostat 10 and febuxostat 15 groups, drug-treated controls; (iv) LPS group, receiving an intraperitoneal injection of LPS (7.5 mg/kg); (v) and (vi) febuxostat 10-LPS and febuxostat 15-LPS groups, receiving oral treatment of febuxostat (10 and 15 mg/kg/day, respectively) for 7 days before LPS. After 18 h administration of LPS, blood was collected for C-reactive protein (CRP) measurement. Bronchoalveolar lavage fluid (BALF) was examined for leukocyte infiltration, lactate dehydrogenase (LDH) activity, protein content, and total nitrate/nitrite. Lung weight gain was determined, and lung tissue homogenate was prepared and evaluated for oxidative stress. Tumor necrosis factor-α (TNF-α) was assessed in BALF and lung homogenate. Moreover, histological changes of lung tissues were evaluated. LPS elicited lung injury characterized by increased lung water content (by 1.2 fold), leukocyte infiltration (by 13 fold), inflammation and oxidative stress (indicated by increased malondialdehyde (MDA), by 3.4 fold), and reduced superoxide dismutase (SOD) activity (by 34 %). Febuxostat dose-dependently decreased LPS-induced lung edema and elevations in BALF protein content, infiltration of leukocytes, and LDH activity. Moreover, the elevated levels of TNF-α in BALF and lung tissue of LPS-treated rats were attenuated by febuxostat pretreatment. Febuxostat also displayed a potent antioxidant activity by decreasing lung tissue levels of MDA and enhancing SOD activity. Histological analysis of lung tissue further demonstrated that febuxostat dose-dependently reversed LPS-induced histopathological changes. These findings demonstrate a significant dose-dependent protection by febuxostat against LPS-induced lung inflammation in rats.
本研究的目的是探讨高效黄嘌呤氧化酶抑制剂非布司他对脂多糖(LPS)诱导的大鼠急性肺损伤(ALI)的可能保护作用。雄性Sprague Dawley大鼠随机分为六组,如下:(i)溶剂对照组;(ii)和(iii)非布司他10组和非布司他15组,药物处理对照组;(iv)LPS组,腹腔注射LPS(7.5 mg/kg);(v)和(vi)非布司他10-LPS组和非布司他15-LPS组,在LPS给药前7天分别口服非布司他(10和15 mg/kg/天)。LPS给药18小时后,采集血液测定C反应蛋白(CRP)。检测支气管肺泡灌洗液(BALF)中的白细胞浸润、乳酸脱氢酶(LDH)活性、蛋白质含量和总硝酸盐/亚硝酸盐。测定肺重量增加,并制备肺组织匀浆并评估氧化应激。评估BALF和肺匀浆中的肿瘤坏死因子-α(TNF-α)。此外,评估肺组织的组织学变化。LPS引起肺损伤,表现为肺含水量增加(1.2倍)、白细胞浸润增加(13倍)、炎症和氧化应激(丙二醛(MDA)增加,3.4倍)以及超氧化物歧化酶(SOD)活性降低(34%)。非布司他剂量依赖性地降低LPS诱导的肺水肿以及BALF中蛋白质含量、白细胞浸润和LDH活性的升高。此外,非布司他预处理减轻了LPS处理大鼠BALF和肺组织中TNF-α水平的升高。非布司他还通过降低肺组织MDA水平和增强SOD活性表现出强大的抗氧化活性。肺组织的组织学分析进一步表明,非布司他剂量依赖性地逆转了LPS诱导的组织病理学变化。这些发现表明非布司他对LPS诱导的大鼠肺部炎症具有显著的剂量依赖性保护作用。