Curcumin promotes oxidative stress, apoptosis and autophagy in H9c2 rat cardiomyoblasts

Molecular & Cellular Toxicology

article

Zepeda-Quiróz, Iván¹  Sánchez-Barrera, Helen¹  Colín-Val, Zaira¹  Robledo-Cadena, Diana Xochiquetzal³  Rodríguez-Enríquez, Sara³  López-Marure, Rebeca¹ 

[1] Departamento de Fisiología, Instituto Nacional de Cardiología “Ignacio Chávez”;Instituto Mexicano del Seguro Social;Departamento de Bioquímica, Instituto Nacional de Cardiología “Ignacio Chávez”

关键词: Curcumin;    Cardiomyoblasts;    Cell cycle;    Oxidative stress;    Cell death;    Mitochondrial damage;    Autophagy;    Mitophagy;   

DOI  :  10.1007/s13273-020-00101-w

来源: Korean Society of Toxicogenomics and Toxicoproteomics

【 摘 要 】

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

【 授权许可】

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