Cell death by hypoxia-acidosis was blocked by pretreatment with antisense BNIP3 oligonucleotides.
The use of polydeoxyribonucleotides (PDRNs) in the treatment of metabolic and/or lactic acidosis conditions is described.
Hypoxia-acidosis-associated cell death is mediated by BNIP3, a member of the Bcl-2 family of apoptosis-regulating proteins.
Additionally, the present invention provides for a method of therapeutic treatment of systemic hypoxia, acidosis, or hypertonicity by administering sickle red blood cells to a patient.
Compounds of this invention, or pharmaceutical compositions thereof, are useful for treating diabetes, elevated plasma glucose levels, and/or ketoacidosis in mammals.
The method comprising administering CO2 to the subject in an amount sufficient to produce an acidotic state in the tissue, the acidotic state serving to prevent alkali damage to the tissue.
The composition simultaneously normalizes the localized ionic environment, thereby normalizing immune responses and reducing acidotic induced pain.