6533b7d2fe1ef96bd125eac4
RESEARCH PRODUCT
Effect of flupirtine on cell death of human umbilical vein endothelial cells induced by reactive oxygen species.
Ralf BohnensackWerner E.g. MüllerGabriela PergandeBernd LorenzThomas Schlütersubject
Programmed cell deathUmbilical VeinsXanthine OxidaseAminopyridinesDNA FragmentationPharmacologyBiochemistryXanthineUmbilical veinchemistry.chemical_compoundNecrosismedicineHumansXanthine oxidaseHypoxanthineCells CulturedPharmacologychemistry.chemical_classificationReactive oxygen speciesCell DeathDose-Response Relationship DrugCell growthchemistryBiochemistryApoptosisCalciumEndothelium VascularFlupirtineReactive Oxygen Speciesmedicine.drugdescription
Abstract Flupirtine (KATADOLON®), known as a nonopiate centrally acting analgesic drug, was tested as to its potential to prevent apoptosis of human endothelial cells induced by reactive oxygen species (ROS). It was found that Flupirtine displayed no effect on viability and cell proliferation of human umbilical vein endothelial cells (HUVEC) up to a concentration of 10 μg/mL. Apoptosis, induced by ROS and generated by hypoxanthine/xanthine oxidase (EC 1.1.3.22) (HX/XOD) or t-butyl hydroperoxide, was reduced after preincubation with Flupirtine for 3 hr by 35% and 41%, respectively. The maximal cytoprotective effect against apoptosis was observed at a drug concentration of 1 to 3 μg/mL. Flow cytometric studies revealed that Flupirtine was able to decrease the number of necrotic cells as well as of apoptotic cells. Neither the simultaneous administration of Flupirtine with the apoptosis-inducing agent nor the preincubation of HUVEC with Flupirtine influenced the increase in the intracellular Ca 2+ concentration [Ca 2+ ] i caused by the production of ROS.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1999-02-11 | Biochemical pharmacology |