Background

Curcumin, a polyphenol derived from Curcuma longa, has some adverse effects on heart; however, its toxic effects on cardiac cells are poorly understood.

Objective

To evaluate the toxicity of curcumin on H9c2 rat cardiomyoblasts. To this, H9c2 cells were exposed to different concentrations of curcumin and proliferation, viability, cell cycle, oxidative stress, mitochondrial membrane potential (ΔΨm), death and autophagy were evaluated.

Results

Curcumin caused concentration-dependent inhibition of H9c2 cells proliferation and viability. A higher sub-G1 population was observed in cells treated with curcumin, which was related with phosphatidylserine translocation and increase of activated caspase-9, indicating apoptotic death. Curcumin induced oxidative stress and decreased ΔΨm causing mitochondrial dysfunction. Additionally, it promoted autophagy, revealed by higher LC3B and beclin-1 protein expression and mitophagy.

Conclusion

Curcumin exhibited toxic effects in cardiac cells and further studies are required to validate its therapeutic potential and use as anti-inflammatory and anti-oxidant agent in the cardiovascular system.

Graphic abstract

中文翻译：

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姜黄素促进H9c2大鼠心肌细胞的氧化应激，细胞凋亡和自噬

背景

姜黄素是源自姜黄的多酚，对心脏有一些不良影响。但是，其对心脏细胞的毒性作用知之甚少。

目的

评估姜黄素对H9c2大鼠心肌母细胞的毒性。为此，将H9c2细胞暴露于不同浓度的姜黄素，并评估其增殖，活力，细胞周期，氧化应激，线粒体膜电位（ΔΨm），死亡和自噬。

结果

姜黄素引起H9c2细胞增殖和活力的浓度依赖性抑制。在用姜黄素处理的细胞中观察到较高的sub-G1群体，这与磷脂酰丝氨酸的转运和活化的caspase-9的增加有关，表明细胞凋亡。姜黄素诱导氧化应激并降低ΔΨm，从而引起线粒体功能障碍。此外，它还促进了自噬，这是由较高的LC3B和beclin-1蛋白表达和线粒体所揭示的。

结论

姜黄素在心脏细胞中表现出毒性作用，需要进一步研究以验证其治疗潜力，并在心血管系统中用作抗炎和抗氧化剂。

图形摘要