Baicalin ameliorates lipopolysaccharide-induced acute lung injury in mice by suppressing oxidative stress and inflammation via the activation of the Nrf2-mediated HO-1 signaling pathway.

Abstract

This research aims to investigate the ameliorative potential of baicalin on lipopolysaccharide-induced acute lung injury by the suppression of oxidative stress and inflammation via the activation of the nuclear erythroid factor 2 (Nrf2)-mediated heme oxygenase-1 (HO-1) signaling pathway. Specific pathogen-free male mice, weighing between 25 and 30g, were divided into the following four groups of 10 mice each: the control group, LPS group, LPS + baicalin group, and baicalin group. Bronchoalveolar lavage fluid (BALF), blood, and tissue were collected on the 16th day and used for hematological (total leukocyte, macrophage, neutrophil, and lymphocyte counts in both blood and BALF, biochemical (antioxidant enzymes, MDA, Nrf2, and HO-1), and histological analyses. The protective effect of baicalin on lipopolysaccharide-induced acute lung injury is based on its antioxidative stress capabilities that are mediated partly by the Nrf2/HO-1 signaling pathway. Baicalin pretreatment significantly decreased the rise in the lung injury score; total leukocyte, neutrophil, lymphocyte, and macrophage counts; pro-inflammatory mediators, tumor necrosis factor (TNF-α), interleukins (IL-6 and IL-1β); biosynthesis of oxidative products, e.g., malondialdehyde (MDA); and restoration of antioxidative enzyme (superoxide dismutase and catalase) activities by improving the expression of nuclear Nrf2 and cytosolic HO-1 in lipopolysaccharide-induced acute lung injury. The protective effects of baicalin are partly due to its antioxidant and anti-inflammatory effects. Our findings indicate that baicalin protects against lipopolysaccharide-induced severe lung injury by enhancing antioxidant systems and significantly reducing both inflammatory cells and mediators via the Nrf2-mediated HO-1 signaling pathway.