PubMed article abstract display

Abstract

Introduction: We aimed to test the mechanism of protective effects of tauroursodeoxycholic acid (TUDCA) on cardiovascular disease using cultured cardiomyocytes.

Methods: Neonatal rat cardiomyocytes (NRCMs) were isolated and cultured and then the cells were divided into 4 groups based on the treatments: control group (cells treated with culture medium), H₂O₂/thapsigargin (TG) group (cells treated with oxidative stress and endoplasmic reticulum [ER] stress inducer), TUDCA group, and H₂O₂/TG + TUDCA group. The treated NRCMs were then subjected to serial analyses including flow cytometry, enzyme-linked immunosorbent assay, and Western blotting.

Results: Tauroursodeoxycholic acid significantly attenuated H₂O₂-induced reactive oxygen species generation and lactate dehydrogenase release and restored H₂O₂-induced reductions of glutathione and superoxide dismutase levels in NRCMs. Tauroursodeoxycholic acid also alleviated H₂O₂-induced cardiomyocytes apoptosis, as well as the Bax/Bcl2 ratio compared with that of H₂O₂ treated alone. In addition, TUDCA suppressed TG-induced ER stress as reflected by inversing cell viability and the expression levels of glucose-regulated protein 78 kDa and C/enhancer-binding protein homologous protein.

Conclusion: Our data indicated that TUDCA-mediated inhibition on H₂O₂-induced oxidative stress and cardiomyocytes apoptosis was through suppressing ER stress, and TUDCA possesses the potential to be developed as therapeutic tool in clinical use for cardiovascular diseases.

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