Role of Calcium Channels in the Protective Effect of Hydrogen Sulfide in Rat Cardiomyoblasts

Cellular Physiology and Biochemistry

关键词: Hydrogen sulfide;    Oxidative stress;    Voltage-operated calcium channels;    Cardiomyoblasts;    Calcium signaling;   

DOI  :  10.1159/000358690

学科分类：分子生物学，细胞生物学和基因

来源: S Karger AG

【 摘 要 】

Background Hydrogen sulfide contributes to the reduction of oxidative stress-related injury in cardiomyocytes but the underlying mechanism is still unclear. Aims Here we investigated the role of voltage-operated calcium channels (VOCCs) as mediators of the beneficial effect of H₂S against oxidative stress in cultured rat cardiomyoblasts (H9c2). Methods Intracellular calcium signals were measured by fluorimetric live cell imaging and cell viability by colorimetric assay. Results Treatment with H₂S donor (NaHS 10 µM) or Nifedipine (10 µM) decreased resting intracellular calcium concentration [Ca]_i, suggesting that L-type VOCCs are negatively modulated by H₂S. In the presence of Nifedipine H₂S was still able to lower [Ca]_i, while co-incubation with Nifedipine and Ni²⁺ 100 µM completely prevented H₂S-dependent [Ca]_i decrease, suggesting that both L-type and T-type VOCCs are inhibited by H₂S. In addition, in the same experimental conditions, H₂S triggered a slow increase of [Ca]_i whose molecular nature remains to be clarified. Pretreatment of H9c2 with NaHS (10 µM) significantly prevented cell death induced by H₂O₂. This effect was mimicked by pretreatment with L-Type calcium channel inhibitor Nifedipine (10 µM). Conclusions The data provide the first evidence that H₂S protects rat cardiomyoblasts against oxidative challenge through the inhibition of L-type calcium channels.

【 授权许可】

CC BY-NC-ND