Molecular Toxicology Laboratory, Department of Biotechnology, Bharathiar University, Coimbatore, Tamil Nadu, 641 046, India.
Cell Stress Chaperones. 2017 Sep;22(5):743-750. doi: 10.1007/s12192-017-0801-1. Epub 2017 Apr 27.
Acute fluoride (F) toxicity is known to cause severe cardiac complications and leads to sudden heart failure. Previously, we reported that increased myocardial oxidative damage, apoptosis, altered cytoskeleton and AMPK signaling proteins associated with energy deprivation in acute F induced cardiac dysfunction. The present study was aimed to decipher the status of myocardial heat shock proteins (Hsps-Hsp27, Hsp32, Hsp40, Hsp60, Hsp70, Hsp90) and heat shock transcription factor 1 (Hsf1) in acute F-intoxicated rats. In order to study the expression of myocardial Hsps, male Wistar rats were treated with single oral doses of 45 and 90 mg/kg F for 24 h. The expression levels of myocardial Hsps were determined using RT-PCR, western blotting, and immunohistochemical studies. Acute F-intoxicated rats showed elevated levels of both the transcripts and protein expression of Hsf1, Hsp27, Hsp32, Hsp60, and Hsp70 when compared to control. In addition, the expression levels of Hsp40 and Hsp90 were significantly declined in a dose-dependent fashion in F-treated animals. Our result suggests that differential expression of Hsps in the rat myocardium could serve as a balance between pro-survival and death signal during acute F-induced heart failure.
急性氟（F）中毒已知会引起严重的心脏并发症，并导致突发性心力衰竭。此前，我们报道了在急性 F 诱导的心脏功能障碍中，心肌氧化损伤增加、细胞凋亡、细胞骨架改变和与能量剥夺相关的 AMPK 信号蛋白。本研究旨在解析急性 F 中毒大鼠心肌热休克蛋白（Hsps-Hsp27、Hsp32、Hsp40、Hsp60、Hsp70、Hsp90）和热休克转录因子 1（Hsf1）的状态。为了研究心肌 Hsps 的表达，雄性 Wistar 大鼠用 45 和 90mg/kg F 进行单次口服处理，24h 后，采用 RT-PCR、western blot 和免疫组化研究测定心肌 Hsps 的表达水平。与对照组相比，急性 F 中毒大鼠的 Hsf1、Hsp27、Hsp32、Hsp60 和 Hsp70 的转录本和蛋白表达水平均升高。此外，在 F 处理的动物中，Hsp40 和 Hsp90 的表达水平呈剂量依赖性显著下降。我们的结果表明，大鼠心肌中 Hsps 的差异表达可能在急性 F 诱导的心力衰竭期间作为生存和死亡信号之间的平衡。
