| Literature DB >> 34617185 |
N V Belosludtseva1, V S Starinets1, K N Belosludtsev2.
Abstract
We studied the effect of a new hypoglycemic compound dapagliflozin on the functioning of rat liver mitochondria. Dapagliflozin in concentrations of 10-20 μM had no effect on the parameters of respiration and oxidative phosphorylation of rat liver mitochondria. Increasing dapagliflozin concentration to 50 μM led to a significant inhibition of mitochondrial respiration in states 3 and 3UDNP. Dapagliflozin in this concentration significantly reduced calcium retention capacity of rat liver mitochondria. These findings indicate a decline in the resistance of rat liver mitochondria to induction of Ca2+-dependent mitochondrial permeability transition pore. In a concentration of 10 μM, dapagliflozin significantly decreases the rate of H2O2 formation in rat liver mitochondria, which attested to an antioxidant effect of this compound. Possible mitochondrion-related mechanisms of the protective action of dapagliflozin on liver cells are discussed.Entities:
Keywords: dapagliflozin; mitochondria; mitochondrial permeability transition pore; mitochondrial respiration; reactive oxygen species
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Year: 2021 PMID： 34617185 PMCID： PMC8494602 DOI： 10.1007/s10517-021-05277-2
Source DB: PubMed Journal: Bull Exp Biol Med ISSN： 0007-4888 Impact factor: 0.804