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硫芥诱导大鼠急性肺损伤后凋亡蛋白和基因的表达

Expressions of apoptotic protein and gene following sulfur mustard-induced acute pulmonary injuries in rats.

作者信息

Liu Tao, Li Jingtong, Hu Xiaoxuan, Tang Jinyuan, Zhong Yuxu, Shu Xin, Zhu Xiao-Ji

机构信息

Department of Respiration, the 80th Group Army Hospital of People's Liberation Army, Weifang, 261021, China.

Department of Pulmonary and Critical Care Medicine, Weifang No. 2 People's Hospital, Weifang Respiratory Disease Hospital, Weifang, 261041, China.

出版信息

Iran J Basic Med Sci. 2025;28(10):1372-1380. doi: 10.22038/ijbms.2025.86449.18678.

DOI:10.22038/ijbms.2025.86449.18678
PMID:40896707
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12399068/
Abstract

OBJECTIVES

Pathomechanisms of sulfur mustard (SM) are not fully understood, and no specific medical countermeasures exist to prevent SM-induced pulmonary injury. This study aimed to evaluate the apoptosis following SM-induced acute pulmonary injury.

MATERIALS AND METHODS

Acute pulmonary injury models were established using SM at an equivalent toxicity dose (1 LD50), administered via intraperitoneal injection or intratracheal instillation. Protein expression levels and mRNA expressions of apoptosis-related markers, including cellular inhibitor of apoptosis proteins-1 and -2 (cIAP-1, cIAP-2), Fas, Bcl-2-associated death promoter (Bad), second mitochondria-derived activator of caspases (Smac), and survivin (BIRC5), were analyzed using immunohistochemistry and polymerase chain reaction.

RESULTS

The intraperitoneal SM group exhibited significantly higher levels of apoptotic cells in the alveolar septa and increased protein and mRNA expression of cIAP-1, cIAP-2, Fas, Bad, Smac, and BIRC5 compared to the intratracheal SM group. These changes displayed a time-dependent increase in both protein and gene expression levels.

CONCLUSION

SM-induced pulmonary injury involves both extrinsic (Fas, cIAP-1, cIAP-2) and intrinsic (Bad, Smac) pathways as well as caspase-dependent pathways (BIRC5). These findings provide valuable insights into the underlying mechanisms of SM toxicity and may facilitate the development of targeted therapeutic strategies.

摘要

目的

硫芥（SM）的发病机制尚未完全明确，且尚无预防SM所致肺损伤的特异性医学对策。本研究旨在评估SM诱导的急性肺损伤后的细胞凋亡情况。

材料与方法

采用等效毒性剂量（1 LD50）的SM通过腹腔注射或气管内滴注建立急性肺损伤模型。使用免疫组织化学和聚合酶链反应分析凋亡相关标志物的蛋白表达水平和mRNA表达，这些标志物包括细胞凋亡抑制蛋白-1和-2（cIAP-1、cIAP-2）、Fas、Bcl-2相关死亡促进因子（Bad）、第二线粒体衍生的半胱天冬酶激活剂（Smac）和生存素（BIRC5）。

结果

与气管内注射SM组相比，腹腔注射SM组肺泡隔中的凋亡细胞水平显著更高，且cIAP-1、cIAP-2、Fas、Bad、Smac和BIRC5的蛋白及mRNA表达增加。这些变化在蛋白和基因表达水平上均呈现出时间依赖性增加。

结论

SM诱导的肺损伤涉及外源性途径（Fas、cIAP-1、cIAP-2）和内源性途径（Bad、Smac）以及半胱天冬酶依赖性途径（BIRC5）。这些发现为SM毒性的潜在机制提供了有价值的见解，并可能有助于开发针对性的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cbe/12399068/e773941cb755/IJBMS-28-1372-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cbe/12399068/459e9576d381/IJBMS-28-1372-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cbe/12399068/475dba77fd78/IJBMS-28-1372-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cbe/12399068/bc2c48247735/IJBMS-28-1372-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cbe/12399068/3a48d16982b6/IJBMS-28-1372-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cbe/12399068/1bc69dd3c19f/IJBMS-28-1372-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cbe/12399068/e773941cb755/IJBMS-28-1372-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cbe/12399068/629b97b53d9d/IJBMS-28-1372-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cbe/12399068/459e9576d381/IJBMS-28-1372-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cbe/12399068/3443e7467379/IJBMS-28-1372-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cbe/12399068/475dba77fd78/IJBMS-28-1372-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cbe/12399068/bc2c48247735/IJBMS-28-1372-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cbe/12399068/3a48d16982b6/IJBMS-28-1372-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cbe/12399068/1bc69dd3c19f/IJBMS-28-1372-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1cbe/12399068/e773941cb755/IJBMS-28-1372-g008.jpg

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Int Immunopharmacol. 2025 Mar 26;150:114285. doi: 10.1016/j.intimp.2025.114285. Epub 2025 Feb 15.
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Oxidative stress reactions in rats with pulmonary injuries induced by sulfur mustard (1 LD).硫芥（1个致死剂量）诱导的肺损伤大鼠的氧化应激反应
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