Multiple analysis of mitochondrial metabolism, autophagy and cell death

In the perspective to evaluate the toxicity of drug candidates or the exploration of intracellular signaling pathways of cell stress response and pathophysiological conditions, we propose to evaluate cell death, autophagy, mitochondrial network and energetic metabolism by a series of optimized joint protocols for neonatal primary rat cardiomyocytes or H9c2 cardiac cell line in 96 well microtiter plates. We used Digitoxigenin and Digoxin, two cardiac glycosides, and Rapamycin as control drugs, for inhibition of oxidative stress-induced cell death and autophagy induction, respectively.