The Effects Of Emodin On Acute Lung Injury

Acute lung injury (ALT) and its more severe form, the acute respiratory distress syndrome (ARDS), are syndromes of acute respiratory fALIure that result from acute pulmonary edema and inflammation. The development of ALI/ARDS is associated with several clinical disorders including direct pulmonary injury from pneumonia and aspiration as well as indirect pulmonary injury from trauma, sepsis, and other disorders such as acute pancreatitis and drug overdose. Although mortality from ALI/ARDS has decreased in the last decade, it remains high. Improved understanding of disease heterogeneity through use of evolving biologic, genomic, and genetic approaches should provide major new insights into pathogenesis of ALL Cellular and molecular methods combined with animal and clinical studies should lead to further progress in the detection and treatment of this complex disease.A major feature of ALI/ARDS that distinguishes it from most other lung diseases such as asthma, chronic obstructive pulmonary disease, and idiopathic pulmonary fibrosis is that ALI/ARDS frequently has systemic components. Furthermore, diffuse injury and infection of the lung are major causes of systemic sepsis and the systemic inflammatory response syndrome and dysregulation of cellular responses in the lung may result in circulating cytokines and other inflammatory, as demonstrated in clinical studies and animal models. Many patients with refractory ALI/ARDS die of multiple organ dysfunction and/or sepsis, rather than isolated progressive respiratory fALIure.Emodin is an important active constituent of many Herbs of traditional Chinese medicines. It has many clinical effects,among which anti-inflammatory is the most important one.Methods: in this study,we setablished ALI anmial and cell model induce by LPS,andobserved the changes of expression of TLR2,TLR4,CD14,SP-A in lung tissues andTHP-1 cell, to proved effects of Emodin on Acute lung injury.Result: The expression of TLR2,TLR4,CD14mRNA and CD14 protein wassignificantly increased in model control group. TLR₂,TLR₄,CD14mRNA of emodingroup significantly decreased and SP-A mRNA expression was also significantlyimproved. Meanwhile, the CD14 protein expression was decreased, the SP-A proteinexpression was increased.Conclusion: Both anmial and cell studies demonstrated new treatments forALI/ARDS. the studies are explore the role of the Emodin in modulating ALI.