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暴露于阿特拉辛会促进心肌细胞灭,通过激活NF-κB通路来加剧心脏毒性
Xuyan Zhao1, Huan Luo2, Sai Yao3
1Institute of Orthopaedics and Traumatology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Traditional Chinese Medicine), Hangzhou 310053, PR China; The Fourth Clinical Medical College of Zhejiang Chinese Medical University, Hangzhou 310053, PR China.
The Science of the total environment
|January 15, 2024
概括
暴露于阿特拉津除草剂会在小鼠中引起心脏纤维化和心肌细胞灭. 这项研究揭示了一种新的机制,通过炎症途径将阿特拉与心脏损伤联系起来.
科学领域:
- 环境毒理学环境毒理学
- 心血管病理学心血管病理学
- 分子毒理学分子毒理学
背景情况:
- 阿特拉是一种广泛使用的除草剂,具有已知的环境持久性.
- 有证据表明,阿特拉会影响多个器官系统,但对心脏的影响尚不清楚.
- 调查阿特拉诱导的心脏损伤的机制对于公共卫生至关重要.
研究的目的:
- 为了阐明特异性毒性和atrazine诱导的心脏损伤的分子机制.
- 为了确定阿特拉津暴露是否导致心脏纤维化和相关的细胞事件.
- 为了探索火灭菌在阿特拉中介心脏损伤中的作用.
主要方法:
- 雄性C57BL/6小鼠在4周和8周内暴露于阿特拉 (50和200毫克/公斤).
- 通过心脏指数,组织病理学和原沉积来评估心脏纤维化.
- 分析了心肌细胞亡,炎症和与亡相关的蛋白质表达 (NLRP3,ASC,CASPASE1,GSDMD).
- 研究了NF-κB通路的激活.
主要成果:
- 阿特拉津暴露显著增加了心脏指数和诱导心脏纤维化与肌纤维损伤.
- 组织病理学揭示了心肌细胞亡,巨细胞透和炎症因子升高.
- 阿特拉辛通过NF-κB通路激活,对关键的烧灭蛋白 (NLRP3,ASC,CASPASE1,GSDMD) 进行了上调.
- 这些分子变化促进了心肌细胞灭.
结论:
- 暴露于阿特拉辛会在小鼠中诱导心脏纤维化.
- 通过NLRP3炎症酶激活和NF-κB信号传递介导的心肌细胞灭是阿特拉诱导的心脏损伤的关键机制.
- 这些发现凸显了阿特拉在心肌纤维化发展中的潜在作用.
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