ALDA-1 treatment and prevention of pulmonary disease
Methods of treating or preventing allergic or pulmonary diseases characterized by endothelial dysfunction with Alda-1 are presented. Treatment of pulmonary endothelial cells subjected to hyperoxia with Alda-1 showed an increase in ALDH2 activity and expression. Treatment with Alda-1 also illustrated a decrease in oxidative stress, a decrease in reactive oxygen species (ROS), a decrease in apoptosis, a decrease in inflammation and an enhancement of mitochondrial membrane potential.
1. A method of treating hyperoxic acute lung injury in a patient in need thereof, the method comprising:
administering a therapeutically effective amount of a composition to the patient in need thereof, the composition comprising
a therapeutically effective amount of Alda-1; and
a pharmaceutically acceptable excipient,
wherein administration of the therapeutically effective amount of the composition containing the Alda-1 enhances activity of ALDH2 and reduces oxidative stress and inflammation in hyperoxic pulmonary cells.
2. The method of claim 1 , wherein the administration of the therapeutically effective amount of the composition containing the Alda-1 rescues mitochondrial membrane potential in the hyperoxic pulmonary cells.
3. The method of claim 1 , wherein the administration of the therapeutically effective amount of the composition containing the Alda-1 decreases apoptosis of the hyperoxic pulmonary cells.
4. The method of claim 1 , wherein the administration of the therapeutically effective amount of the composition containing the Alda-1 suppresses mitochondrial reactive oxygen species (ROS) production in the hyperoxic pulmonary cells.
5. The method of claim 1 , wherein administration of the therapeutically effective amount of the composition containing the Alda-1 increases mitochondrial membrane potential in the hyperoxic pulmonary cells.
6. The method of claim 1 , wherein the administration of the therapeutically effective amount of the composition containing the Alda-1 decreases accumulation of 4-hydroxy-2-noneal (4HNE) in the hyperoxic pulmonary cells.