ABSTRACT

Conclusion:

We found that TRPM2 channels are overactivated during paclitaxel induced cardiotoxicity and NAC could show a cardioprotective effect through TRPM2 channel modulation.

Results:

Cytosolic calcium levels, apoptosis levels, intracellular ROS production levels were lower in paclitaxel+NAC group than in the paclitaxel group of cardiomyocytes. Also values were markedly lower in the paclitaxel+NAC+antranilic acid group when compared to the paclitaxel+NAC group.

Material and Methods:

All cells were cultured at 37°C. The cells were divided into seven main groups. Cells in the paclitaxel group were incubated with 2.5 μM Paclitaxel for 12 hours and cells in the NAC+Paclitaxel group were incubated with 2.5 μM Paclitaxel for 12 hours and then incubated with 10 μM NAC for 24 hours. Intracellular free calcium concentration , reactive oxygen species (ROS) production measurements and cell viability analyses were done according to the study protocol.

Aim:

In our study ,we investigated the paclitaxel induced cardiotoxicity and alterations in Ca2+ influx , oxidative stress and apoptosis through transient receptor potential melastatin 2 (TRPM2) channels and modulator role of Nacetyl cysteine (NAC) in cardiomyocytes.