Abstract
Acute lung injury (ALI) and its severe manifestation of acute respiratory distress syndrome (ARDS) are well-known illnesses. Uncontrolled and self-amplified pulmonary inflammation lies at the center of the pathology of this disease. Emodin, the bio-active coxund of herb Radix rhizoma Rhei, shows potent anti-inflammatory properties through inactivation of nuclear factor-κB (NF-κB). The aim of this study was to evaluate the effect of emodin on lipopolysaccharide (LPS)-induced ALI in mice, and its potential bio-mechanism. In our study, BALB/c mice were stimulated with LPS to induce ALI. After 72 h of LPS stimulation, pulmonary pathological changes, lung injury scores, pulmonary edema, myeloperoxidase (MPO) activity, total cells, neutrophils, macrophages, TNF-α, IL-6 and IL-1β in bronchoalveolar lavage fluid (BALF), and MCP-1 and E-selectin expression were notably attenuated by emodin in mice. Meanwhile, our data also revealed that emodin significantly inhibited the LPS-enhanced the phosphorylation of NF-κB p65 and NF-κB p65 DNA binding activity in lung. Our data indicates that emodin potently inhibits LPS-induced pulmonary inflammation, pulmonary edema and MCP-1 and E-selectin expression, and that these effects were very likely mediated by inactivation of NF-κB in mice. These results suggest a therapeutic potential of emodin as an anti-inflammatory agent for ALI/ARDS treatment.
Highlights
Acute lung injury (ALI) and its severe manifestation, acute respiratory distress syndrome (ARDS), are well-known fatal diseases with an extremely high morbidity rate (35% to 50%) in critically ill patients [1,2,3]
The lung injury scores and wet to dry ratio (W/D) were both markedly attenuated by emodin intervention
No difference in lung injury scores and W/D was found between the Control group and the Emodin group
Summary
Acute lung injury (ALI) and its severe manifestation, acute respiratory distress syndrome (ARDS), are well-known fatal diseases with an extremely high morbidity rate (35% to 50%) in critically ill patients [1,2,3]. The multiple etiologies, including severe sepsis, pneumonia, lung abscess and severe burn, cause uncontrolled and self-amplified pulmonary inflammation which lie at the center of the pathology of ALI/ARDS [2,10,11,12,13,14,15,16]. The NF-κB signaling pathway plays a critical role in the inflammatory processes in ALI/ARDS [15,17,18,19,20]. Reports demonstrated that the severity of inflammation in ALI/ARDS was greatly reduced by inhibition of the NF-κB signaling pathway [15,17,18,19,20]. Multiple studies demonstrated that the NF-κB signaling pathway is a promising therapeutic target of ALI/ARDS and other inflammatory diseases, including arthritis, pulmonary fibrosis, asthma and hepatitis [17,18,21]
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