Abstract
Acute lung injury (ALI) is a common respiratory disease characterized by the alveolar edema and pulmonary inflammation, which results in the respiratory failure and even death. The current research study was planned to assess the beneficial properties of rubusoside against the LPS-provoked ALI in mice through the alleviation of oxidative stress and inflammatory responses. The viability of lipopolysaccharide (LPS)-provoked RAW 264.7 cells were assessed by MTT assay. The ALI was initiated to the mice via administering the LPS (5 mg/kg) for 3 days and supplemented with the 30 mg/kg of rubusoside. The lung edema, total cells, and protein content were assessed by standard methods. The pro-inflammatory markers level was investigated by assay kits and the antioxidant biomarkers were analyzed by standard techniques. The levels of inflammatory biomarkers in the LPS-provoked RAW 264.7 cells and lung tissues of ALI mice were studied by RT-PCR assay. The lung tissues were analyzed microscopically to identify the histological alterations. The rubusoside treatment effectively decreased the RAW 264.7 cells viability. The rubusoside also inhibited the lung edema, IL-6, and TNF-alpha content, ROS accumulation, and TBARS level in the LPS-challenged ALI mice. Rubusoside also improved the GSH content and CAT activity in the ALI mice. The levels of TLR-4, COX-2, iNOS, and IL-1 beta were effectively down-regulated by the rubusoside in both LPS-challenged RAW 264.7 cells and lung tissues. The finding of lung tissue histopathology was also proved the therapeutic action of rubusoside. Altogether, our results suggest that rubusoside demonstrates therapeutic property against the LPS-challenged ALI in mice via inhibiting the inflammatory responses and it can be an effective drug to treat the ALI in future.