Abstract
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 H<sub>2</sub>S 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 H<sub>2</sub>S donor (NaHS 10 µM) or Nifedipine (10 µM) decreased resting intracellular calcium concentration [Ca]<sub>i</sub>, suggesting that L-type VOCCs are negatively modulated by H<sub>2</sub>S. In the presence of Nifedipine H<sub>2</sub>S was still able to lower [Ca]<sub>i</sub>, while co-incubation with Nifedipine and Ni<sup>2+</sup> 100 µM completely prevented H<sub>2</sub>S-dependent [Ca]<sub>i</sub> decrease, suggesting that both L-type and T-type VOCCs are inhibited by H<sub>2</sub>S. In addition, in the same experimental conditions, H<sub>2</sub>S triggered a slow increase of [Ca]<sub>i</sub> whose molecular nature remains to be clarified. Pretreatment of H9c2 with NaHS (10 µM) significantly prevented cell death induced by H<sub>2</sub>O<sub>2</sub>. This effect was mimicked by pretreatment with L-Type calcium channel inhibitor Nifedipine (10 µM). Conclusions: The data provide the first evidence that H<sub>2</sub>S protects rat cardiomyoblasts against oxidative challenge through the inhibition of L-type calcium channels.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
