Glycyrrhizic acid alleviates the meconium-induced acute lung injury in neonatal rats by inhibiting oxidative stress through mediating the Keap1/Nrf2/HO-1 signal pathway

Meconium aspiration syndrome (MAS) is a disease closely related to inflammation and oxidative stress. Glycyrrhizic acid (GA) is a triterpenoid isolated from licorice with multiple bioprotective properties. In the present study, impacts of GA against MAS rats, as well as the potential mechanism, will be investigated. MAS model was established on newborn rats, followed by the treatment of 12.5, 25, and 50 mg/kg GA. The wet/dry weight ratio of lung tissues was calculated. The production of IL-6, IL-1β, TNF-α, malonaldehyde (MDA), superoxide dismutase (SOD), glutathione (GSH) was measured using ELISA assay. HE staining was used to evaluate the pathological state of lung tissues and TUNEL assay was used to detect the apoptotic state. The protein expression of Nrf2, Keap1, HO-1, Bcl-2, Bax, and cleaved-Caspase3 was measured by Western blotting assay. The elevated W/D ratio, release of inflammatory factors, lung injury score, and apoptotic index, as well as the activated oxidative stress and suppressed Keap1/Nrf2/HO-1 pathway, in MAS rats were significantly alleviated by GA. After introducing the inhibitor of Nrf2, ML385, the protective property of GA on the pathological state, apoptotic index, and oxidative stress in MAS rats was pronouncedly abolished. Taken together, glycyrrhizin alleviated GAH in rats by suppressing Keap1/Nrf2/HO-1 signaling mediated oxidative stress.