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吸入一氧化氮可提高百草枯中毒大鼠的存活率。

Inhaled nitric oxide improves the survival of the paraquat-injured rats.

作者信息

Cho Jae Hwa, Yang Doo Kyung, Kim Lucia, Ryu Jeong Seon, Lee Hong Lyeol, Lim Chae Man, Koh Youn Suck

机构信息

Division of Pulmonology and Critical Care Medicine, Department of Internal Medicine, College of Medicine, Inha University, Incheon, Republic of Korea.

出版信息

Vascul Pharmacol. 2005 Mar;42(4):171-8. doi: 10.1016/j.vph.2005.01.001.

DOI:10.1016/j.vph.2005.01.001
PMID:15820443
Abstract

The purpose of this study was to evaluate the effects of inhaled nitric oxide (NO) on the paraquat-induced lung injury in rats. The rats were assigned to four groups: control; inhaled NO (5 ppm); paraquat (PQ, 30 mg/kg); and PQ+NO group. For first 18 h the inhalation of NO mixed with room air was performed. Total white blood cell (WBC), neutrophil, total protein, lactate dehydrogenase (LDH), transforming growth factor-beta1 (TGF-beta1) in serum and/or bronchoalveolar lavage (BAL) fluid, serum malonaldehyde (MDA), and myeloperoxidase (MPO) of lung were measured and lung histopathology were also reviewed. The 72-h survival rate of PQ group was 58%, but the survival rate of PQ+NO group, NO group and control group were 100%, respectively. The serum MDA and TGF-beta1 in BAL fluid and blood of PQ+NO group were significantly lower than those of PQ group. However, inhaled NO did not decrease the elevated total WBC and neutrophil counts, and total protein, LDH and MPO activity in the lung injured by PQ. The alveolar septal thickening and inflammatory cell infiltration were not different between PQ and PQ+NO groups. NO inhalation may be beneficial for the survival of paraquat-induced injured rats by attenuating lipid peroxidation and production of TGF-beta1.

摘要

本研究的目的是评估吸入一氧化氮(NO)对百草枯诱导的大鼠肺损伤的影响。将大鼠分为四组:对照组;吸入NO(5 ppm)组;百草枯(PQ,30 mg/kg)组;以及PQ+NO组。在最初的18小时内进行NO与室内空气混合的吸入操作。检测血清和/或支气管肺泡灌洗(BAL)液中的总白细胞(WBC)、中性粒细胞、总蛋白、乳酸脱氢酶(LDH)、转化生长因子-β1(TGF-β1),血清丙二醛(MDA)以及肺组织中的髓过氧化物酶(MPO),并对肺组织病理学进行评估。PQ组的72小时生存率为58%,而PQ+NO组、NO组和对照组的生存率分别为100%。PQ+NO组BAL液和血液中的血清MDA和TGF-β1显著低于PQ组。然而,吸入NO并未降低PQ所致肺损伤中升高的总WBC和中性粒细胞计数,以及总蛋白、LDH和MPO活性。PQ组和PQ+NO组之间的肺泡间隔增厚和炎症细胞浸润无差异。吸入NO可能通过减轻脂质过氧化和TGF-β1的产生而有利于百草枯诱导的损伤大鼠的存活。

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Inhaled nitric oxide improves the survival of the paraquat-injured rats.吸入一氧化氮可提高百草枯中毒大鼠的存活率。
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引用本文的文献

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Pharmacological inhibition of CXCR2 chemokine receptors modulates paraquat-induced intoxication in rats.CXCR2趋化因子受体的药理学抑制作用可调节百草枯诱导的大鼠中毒。
PLoS One. 2014 Aug 25;9(8):e105740. doi: 10.1371/journal.pone.0105740. eCollection 2014.
2
Complement inhibition alleviates paraquat-induced acute lung injury.补体抑制可减轻百草枯诱导的急性肺损伤。
Am J Respir Cell Mol Biol. 2011 Oct;45(4):834-42. doi: 10.1165/rcmb.2010-0444OC. Epub 2011 Mar 18.
3
Curcumin enhances paraquat-induced apoptosis of N27 mesencephalic cells via the generation of reactive oxygen species.
姜黄素通过产生活性氧增强百草枯诱导的 N27 中脑细胞凋亡。
Neurotoxicology. 2009 Nov;30(6):1008-18. doi: 10.1016/j.neuro.2009.07.016. Epub 2009 Aug 4.
4
Nitric oxide-mediated toxicity in paraquat-exposed SH-SY5Y cells: a protective role of 7-nitroindazole.硝普钠介导的百草枯染毒 SH-SY5Y 细胞毒性:7-硝基吲唑的保护作用。
Neurotox Res. 2009 Aug;16(2):160-73. doi: 10.1007/s12640-009-9065-6. Epub 2009 May 30.