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酸盐通过线粒体激活蛋白激酶介导的氧化应激和炎症诱导急性肺损伤

Sangryul Cha¹, Jooyeon Lee¹, Jimin Jang¹

¹Department of Thoracic and Cardiovascular Surgery, Kangwon National University, Chuncheon, Gangwon State 24341, Republic of Korea.

Ecotoxicology and environmental safety

|September 26, 2025

概括

酸盐通过增加氧化应激和激活MAPK通路而导致肺损伤. 准这种途径可能有助于治疗重金属诱导的肺损伤.

科学领域:

毒理学毒理学毒理学
分子生物学分子生物学
环境健康环境健康

背景情况:

酸盐 (Na2CrO4) 是一种具有已知的肺毒性工业化学物质.
Na2CrO4诱导的急性肺损伤 (ALI) 的分子机制尚未完全理解.
研究氧化应激和炎症途径对于理解Na2CrO4毒性至关重要.

研究的目的:

阐明Na2CrO4诱导的肺毒性的分子机制.
研究氧化应激和炎症信号通路 (NF-κB,MAPK) 在Na2CrO4诱导的ALI中的作用.
评估针对这些途径的治疗潜力.

主要方法:

在体内使用C57BL/6小鼠暴露于Na2CrO4.4的研究.
在体外研究中,使用使用Na2CrO4.4治疗的MLE-12膜上皮细胞进行了实验.
使用了组织学分析,BALF采集,ELISA,西部抹杀和特定途径抑制剂.

主要成果:

暴露于Na2CrO4引起了急性肺炎,其特征是中性粒细胞透和IL-6和TNF-α水平升高.
观察到显著的氧化应激和MAPK信号通路的强烈激活.
NF-κB激活是有限的,而MAPK通路激活则是Na2CrO4诱导的肺毒性的核心.

结论:

氧化应激和MAPK通路激活是Na2CrO4诱导的肺毒性的关键机制.
针对MAPK信号通路显示了减轻重金属诱导的肺损伤的潜力.
对Na2CrO4的环境暴露对公众健康构成重大风险.

关键词:

在MAPK路径激活过程中.这就是Na2CrO4的含量.Na2CrO4引起的急性肺损伤 (ALI)肺部有毒性肺部有毒性

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