One of the leading causes of
acute lung injury, which is linked to a high death rate, is pulmonary
fat embolism. Increases in proinflammatory
cytokines and the production of
free radicals are related to the pathophysiology of
acute lung injury.
Antioxidants that scavenge
free radicals play a protective role against
acute lung injury.
Gossypin has been proven to have
antioxidant, antimicrobial, and anti-inflammatory properties. In this study, we compared the role of
Gossypin with the therapeutically used
drug Dexamethasone in the
acute lung injury model caused by
oleic acid in rats. Thirty rats were divided into five groups;
Sham,
Oleic acid model, Oleic acid+Dexamethasone (0.1 mg/kg), Oleic acid+Gossypin (10 and 20 mg/kg). Two hours after pretreatment with
Dexamethasone or
Gossypin, the
acute lung injury model was created by injecting 1 g/kg
oleic acid into the femoral vein. Three hours following the
oleic acid injection, rats were decapitated. Lung tissues were extracted for histological, immunohistochemical, biochemical, PCR, and SEM imaging assessment. The
oleic acid injection caused an increase in lipid peroxidation and
catalase activity, pathological changes in lung tissue, decreased
superoxide dismutase activity, and
glutathione level, and increased TNF-α, IL-1β,
IL-6, and
IL-8 expression. However, these changes were attenuated
after treatment with
Gossypin and
Dexamethasone. By reducing the expression of proinflammatory
cytokines and attenuating oxidative stress,
Gossypin pretreatment provides a new target that is equally effective as
dexamethasone in the treatment of
oleic acid-induced
acute lung injury.