Effect of Dapagliflozin on the Functioning of Rat Liver Mitochondria In Vitro
We studied the consequence of new hypoglycemic compound dapagliflozin around the functioning of rat liver mitochondria. Dapagliflozin in concentrations of 10-20 µM didn’t have impact on the parameters of respiration and oxidative phosphorylation of rat liver mitochondria. Growing dapagliflozin concentration to 50 µM brought to some significant inhibition of mitochondrial respiration in states 3 and 3UDNP. Dapagliflozin within this concentration considerably reduced calcium retention capacity of rat liver mitochondria. These bits of information indicate a loss of the resistance of rat liver mitochondria to Dapagliflozin induction of Ca2 -dependent mitochondrial permeability transition pore. Inside a power of 10 µM, dapagliflozin considerably lessens the rate of H2O2 formation in rat liver mitochondria, which attested for an antioxidant aftereffect of this compound. Possible mitochondrion-related mechanisms from the protective action of dapagliflozin on liver cells are discussed.