Prophylaxis Against Lipopolysaccharide-Induced Lung Injuries by Liposome-Entrapped Dexamethasone in Rats


  1. Suntres, Z.E.
  2. Shek, P.N.
Corporate Authors
Defence and Civil Inst of Environmental Medicine, Downsview ONT (CAN)
Lipopolysaccharide (LPS), a component of the cell wall of Gram-negative bacteria, stimulates phagocytes to generate metabolites that play an important role in the pathogenesis of acute lung injury. In this study, the prophylatic effect of liposome-entrapped dexamethasone (L-DEX) was evaluated in an animal acute lung injury model. Rats were pretreated intratracheally with L-DEX or dexamethasone phosphate (DEX) at a dose of 800 mu g dexamethasone/kg body weight; 1 hr later, pretreated animals were challenged i.v. with LPS (Escherichia coli 0111:B4, 1 mg/kg body weight) and killed 24 hr later. Challenge of saline-pretreated animals with LPS resulted in lung injury, as evidenced by increases in wet lung weight and decreases in lung angiotensin-converting enzyme and alkaline phosphatase activities, injury markers of pulmonary capillary endothelial and alveolar type II epithelial cells, respectively. Also, LPS injection resulted in significant increases in plasma phospholipase A2, thromboxane B2, and leukotriene B4, concentrations. The LPS challenge also increased pulmonary myeloperoxidase and elastase activities as well as chloramine concentration, suggestive of neutrophil infiltration and activation of the inflammatory response. TRUNCATED
Drug delivery;Lung injuries;Dexamethasone;Acute lung injury;Sepsis;Inflammation
Report Number
DCIEM-SL-1999-060 — Reprint
Date of publication
20 Sep 1999
Number of Pages
Reprinted from
Biochemical Pharmacology, vol 59, 2000, p 1155-1161
Hardcopy;Document Image stored on Optical Disk

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