Gossypin mitigates oxidative damage by downregulating the molecular signaling pathway in oleic acid-induced acute lung injury

Abstract

One of the leading causes of acute lung injury, which is linked to a high death rate, is pul-monary fat embolism. Increases in proinflammatory cytokines and the production of freeradicals are related to the pathophysiology of acute lung injury. Antioxidants that scav-enge free radicals play a protective role against acute lung injury. Gossypin has beenproven to have antioxidant, antimicrobial, and anti-inflammatory properties. In this study,we compared the role of Gossypin with the therapeutically used drug Dexamethasonein the acute lung injury model caused by oleic acid in rats. Thirty rats were divided intofive 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 orGossypin, the acute lung injury model was created by injecting 1 g/kg oleic acid into thefemoral vein. Three hours following the oleicacid injection, rats were decapitated. Lungtissues were extracted for histological, immunohistochemical, biochemical, PCR, andSEM imaging assessment. The oleic acid injection caused an increase in lipid peroxidationand catalase activity, pathological changes in lung tissue, decreased superoxide dismu-tase 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 Dexameth-asone. By reducing the expression of proinflammatory cytokines and attenuating oxida-tive stress, Gossypin pretreatment provides a new target that is equally effective asdexamethasone in the treatment of oleic acid-induced acute lung injury