Abstract
The present study aimed to investigate the protective effects of ganoderic acid A (GAA) on lipopolysaccharide (LPS)-induced acute lung injury. In mouse model of LPS-induced acute lung injury, we found that GAA led to significantly lower lung wet-to-dry weight ratio and lung myeloperoxidase activity, and attenuated pathological damages. In addition, GAA increased superoxide dismutase activity, but decreased malondialdehyde content and proinflammatory cytokines levels in the bronchoalveolar lavage fluid. Mechanistically, GAA reduced the activation of Rho/ROCK/NF-κB pathway to inhibit LPS-induced inflammation. In conclusion, our study suggests that GAA attenuates acute lung injury in mouse model via the inhibition of Rho/ROCK/NF-κB pathway.
Highlights
Acute lung injury (ALI) has a high mortality of up to 40% and is a serious respiratory disease characterized by neutrophils infiltration, pulmonary edema, and inflammation [1]
We examined the protective effects of Ganoderic acid A (GAA) on LPS-induced acute lung injury and explored whether these effects are related to the inhibition of Rho/ROCK/NF-κB pathway
GAA treatment led to lower wet-to dry (W/D) weight ratio in model group (Figure 1)
Summary
Acute lung injury (ALI) has a high mortality of up to 40% and is a serious respiratory disease characterized by neutrophils infiltration, pulmonary edema, and inflammation [1]. While the pathogenesis of ALI remains unclear, it is accepted that during ALI the injury of the alveolar epithelium and capillary endothelium would cause airspace edema and inflammation due to increased alveolar barrier permeability [1]. Ganoderic acid A (GAA) is one of triterpenoid extracts of G. lucidum with a range of biological activities [2,3]. A recent study reported that GAA has anti-inflammation activity to inhibit lipopolysaccharide (LPS)-induced secretion of inflammatory cytokine [4]. The efficacy of GAA to treat LPS-induced lung injury remains unclear
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