Thioredoxin prevents the development and progression of elastase-induced emphysema
Thioredoxin prevents the development and progression of elastase-induced emphysema
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DOI：
10.1016/j.bbrc.2007.01.053
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发表时间：
2007-03-16
影响因子：
3.1
通讯作者：
Aizawa, Hisamichi
中科院分区：
文献类型：
--
作者：
Kinoshita, Takashi;Hoshino, Tomoaki;Aizawa, Hisamichi
硫氧还蛋白I（TRX 1）是一种氧化还原（还原/氧化）活性蛋白，可清除活性氧。在这里，我们研究了内源性或外源性TRX 1的管理是否阻止弹性蛋白酶诱导的肺气肿的发展和进展。在第0天通过微喷雾用气管内弹性蛋白酶处理小鼠，并从第-1至21天每隔一天给予重组人TRX 1（rhTRX 1）。为了确定TRX 1对已建立的肺气肿进展的影响，在第0天用弹性蛋白酶对小鼠进行气管内处理，并从第14天至第21天施用rhTRX 1。在第21天进行组织学检查。TRX 1转基因但非转基因阴性小鼠表现出弹性蛋白酶诱导的肺气肿的生理指标降低。从第-1天到第19天的TRX 1给药显著减少了弹性蛋白酶诱导的肺气肿的体征。此外，在弹性蛋白酶治疗后14天开始给予TRX 1显著减缓了肺气肿的进展。TRX 1可能对COPD的治疗具有临床益处。(c)2007 Elsevier lnc. All rights reserved.
Thioredoxin I (TRX1) is a redox (reduction/oxidation) -active protein that scavenges reactive oxygen species. Here we examined whether endogenous or exogenous administration of TRX1 prevented the development and progression of elastase-induced pulmonary emphysema. Mice were treated with intratracheal elastase via microspray on day 0, and were given recombinant human TRX1 (rhTRX1) every other day from days -1 to 21. To determine the effects of TRX1 on the progression of established emphysema, mice were treated intratracheally with elastase on day 0, and rhTRX1 was administered from days 14 to 21. Histopathologic examination was performed on day 21. TRX1-transgenic but not transgene-negative mice demonstrated a decrease in the physiological indicators of elastase-induced emphysema. TRX1 administration from days -1 to 19 significantly decreased the signs of elastase-induced emphysema. Moreover, TRX1 administration beginning 14 days after elastase treatment significantly slowed the progression of emphysema. TRX1 may be of clinical benefit for the treatment of COPD. (c) 2007 Elsevier lnc. All rights reserved.