Betanin ameliorates Lipopolysaccharide-induced acute lung injury in mice via inhibition of inflammatory response and oxidative stress

Abstract

BackgroundAcute lung injury (ALI) is the most common form of inflammatory disease, which has higher morbidity and mortality rates worldwide. ALI is characterized by alterations in the lungs such as epithelial dysfunction, excessive inflammation, and lung edema. ObjectiveThe current work was aimed to unveil the abrogative properties of betanin on the LPS-induced ALI in mice. MethodologyIn an in vitro assay, betanin-treated RAW 264.7 cells viability was evaluated by MTT assay. The TNF-α, IL-1β, and IL-6 levels in the cell lysates were estimated using assay kits. In in vivo studies, the ALI was initiated in the BALB/c mice by exposing them to a 3-day intra-tracheal challenge of 5 mg/kg of LPS and then treated with betanin (25 and 50 mg/kg) for three days. Later, the BALF samples were obtained from the mice and used to estimate the inflammatory biomarkers using assay kits. The levels of MDA and the antioxidants SOD and GSH were also examined using commerical kits. The iNOS, COX-2, and PGE-2 expressions were estimated using kits, and finally the histopathological study was conducted on the lung tissues. ResultsThe outcomes of in vitro studies revealed that betanin appreciably improved the viability of LPS-exposed RAW 264.7 cells. The betanin effectively diminished the levels of IL-6, IL-1β, and TNF-α in LPS-induced RAW 264.7 cells. In in vivo studies, the findings demonstrated that betanin treatment diminished the lung/bodyweight, lung W/D weight, and protein level in the ALI mice. The inflammatory cell counts and inflammatory biomarkers such as COX-2, PGE2, and iNOS were substantially reduced by the betanin treatment in the ALI mice. Betanin treatment also increased the GSH and SOD and reduced the MDA in the ALI mice. The histopathological alterations in the lungs tissues of ALI mice were effectively ameliorated by the betanin. ConclusionIn summary, the findings apparently suggest that betanin effectively ameliorated the LPS-triggered ALI in mice through its beneficial properties. Therefore, in the future, it can be used as a new salutary candidate to manage the ALI in medical settings.