The effects of melatonin on oxidative stress, inflammation, apoptosis and Nrf2/HO-1 in acrylamide-induced lung injury in rats.

This study is to investigate the effects of melatonin on lung inflammation, oxidative stress, apoptosis, tissue damage, and MT1 and MT2 receptors in acrylamide-induced lung toxicity. Fifty male rats were randomly divided into five groups. The control group received distilled water orally for 11 days, while the acrylamide group received acrylamide (50 mg/kg, i.g.) for 11 days. The MEL10 + ACR and MEL20 + ACR groups received intraperitoneal injections of melatonin at doses of 10 mg/kg and 20 mg/kg, respectively, followed by acrylamide (50 mg/kg, i.g.) administered 1 h after melatonin injection. The MEL20 group received melatonin injections (20 mg/kg) for 11 days. Lung tissues collected at the end of the study underwent biochemical, histopathological, immunohistochemical, immunofluorescence, and in silico analyses. Acrylamide caused oxidative stress, inflammation, apoptosis, and tissue damage in the lungs. Melatonin treatment alleviated acrylamide-induced lung damage by exhibiting antioxidant, anti-inflammatory, and anti-apoptotic effects. Melatonin significantly improved the histopathological changes caused by acrylamide in lung tissue. Melatonin may have protective effects on health by regulating cellular processes such as oxidative stress, antioxidant enzyme activity, inflammation, and apoptosis through MT1 and MT2 receptors. Melatonin mitigates oxidative stress, inflammation, apoptosis, and tissue damage in acrylamide-induced lung injury in rats.