Abstract
Sepsis is an intense immune response to infection that contributes to the pathophysiological process of acute lung injury (ALI). Inflammation and oxidative stress serve an important role in the development of ALI. Leonurine (LEO) is a natural phenolic alkaloid extracted from Leonurus cardiaca, which possesses anti-inflammatory and antioxidative properties. Therefore, the aim of the present study was to explore the effect of LEO on sepsis-induced ALI and to investigate its underlying mechanism. MTT and Cell Counting Kit-8 assays were performed to measure cell viability. The levels of reactive oxygen species, lactate dehydrogenase and malondialdehyde, as well as the activity of superoxidase dismutase, were quantified using commercial assay kits. The expression levels of specific inflammatory cytokines were measured by using ELISA. In addition, western blotting was employed to assess the expression levels of cytokines, including TNF-α, IL-6, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1. The findings demonstrated that LEO increased the viability of lipopolysaccharide (LPS)-stimulated BEAS-2B human lung epithelial cells in a dose-dependent manner. Additionally, LEO suppressed LPS-induced oxidative stress and inflammatory cytokine release in BEAS-2B cells. Treatment with Nrf2 inhibitor reversed the effects of LEO treatment on LPS-induced oxidative stress and inflammatory response in BEAS-2B cells. Taken together, the data of the present study indicated that LEO attenuated LPS-induced ALI through the inhibition of oxidative stress and inflammation regulated by the Nrf2 signaling pathway. Therefore, LEO may be a novel and effective agent for the prevention of sepsis-induced ALI.