脏中的前林因表达增加可能与长期暴露于微囊素-LR的环境引起的异常功能有关
Yuuka Hitsuda1, Yoshihito Koto1, Hideaki Kawahara2
1Graduate School of Natural Science and Technology, Shimane University, 1060 Nishikawatsu-Cho, Matsue 690-8504, Japan.
Toxics
|August 28, 2024
概括
长期口服暴露于有害藻类繁殖中的毒素microcystin-LR,显著增加了老鼠脏中的prorenin表达. 这可能会通过影响相关的分子通路来启动纤维化和功能障碍.
科学领域:
- 环境毒理学环境毒理学
- 腎臟病學 (nephrology) 是一種醫學.
- 分子生物学分子生物学
背景情况:
- 欧湖是产生微囊的有毒藻类的息地,造成环境和健康风险.
- 之前关于微囊素-LR对的影响的研究使用非口服暴露,缺乏分子机制的洞察力.
- 口服暴露研究主要评估功能和病理,而不是潜在的分子变化.
研究的目的:
- 为了研究口服后微囊素LR诱导的损伤的分子机制.
- 为了评估慢性口服微囊素-LR暴露对脏近端管状细胞的影响.
- 探索前列宁表达与脏中关键纤维化标志物之间的关系.
主要方法:
- 微囊素-LR口服给WKAH/HkmSlc大鼠7周时间.
- 对功能等离子体标志物的分析 (白蛋白,BUN,肌).
- 在皮和近端管状细胞中对前列宁, (前列宁受体 (PRR),TGFβ1和α-SMA的基因表达的量化.
主要成果:
- 在对照组和微囊素-LR组之间,血白蛋白,BUN或肌蛋白没有显著差异.
- 在接受微囊素LR治疗的老鼠的皮和近端管状细胞中显著增加了前列宁表达.
- 在皮质中,prorenin表达与PRR,TGFβ1和α-SMA显著正相关.
结论:
- 慢性口服微囊素-LR暴露会增加脏前列宁的表达,而不会改变标准的功能标志物.
- 增加的前列宁可以通过调节PRR,TGFβ1和α-SMA来启动纤维化和功能障碍.
- 这项研究阐明了通过口服暴露的微囊素-LR毒性潜在的分子途径.
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