SPRC protects hypoxia and re-oxygenation injury by improving rat cardiac contractile function and intracellular calcium handling

- SPRC can against cardiac hypoxia/re-oxygenation injury.
- In isolated papillary muscles, SPRC can attenuated the apoptosis cause by H/R.
- In isolated myocytes, it can recovery the cell function after H/R.
- SPRC exerts protective effects by reducing Ca2+ overload.
- These protect effects can partly block by the CSE inhibitor PAG.

S-Propargyl-l-cysteine (SPRC, also named as ZYZ-802) is a new compound synthesized in our lab. We investigated whether SPRC has exerted protective effects against cardiac hypoxia/re-oxygenation (H/R) and also explored its mechanisms. In our study, isolated ventricular myocytes were subject to a simulated hypoxia solution for 30 min to induce cell injury. Intracellular concentration of Ca2+ ([Ca2+]i) was measured using specific dyes and detected by digital imaging apparatus. Apoptotic cells were evaluated by TUNEL assay. Intervention with SPRC (10 μM) 30 min before hypoxia, can significantly attenuate the apoptosis of isolated papillary muscles resulting from the H/R injury and protect morphology of the muscles. In isolated ventricular myocytes, SPRC considerably improved left ventricular functional recovery. SPRC also suppressed the increase of ([Ca2+]i) during hypoxia stage. By measuring the calcium transient of the cell we concluded that SPRC can preserve the RyR and SERCA activities and improve Ca2+ handling during the H/R. Furthermore, the protective effect of SPRC can be partly blocked by CSE inhibitor PAG.