Escin attenuates acute lung injury induced by endotoxin in mice.
Endotoxin causes multiple organ dysfunctions, including acute lung injury (ALI). The current therapeutic strategies for endotoxemia are designed to neutralize one or more of the inflammatory mediators. Accumulating experimental evidence suggests that escin exerts anti-inflammatory and anti-edematous effects. The aim of this study was to evaluate the effect of escin on ALI induced by endotoxin in mice. ALI was induced by injection of lipopolysaccharide (LPS) intravenously. The mice were given dexamethasone or escin before injection of LPS. The mortality rate was recorded. Tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β) and nitric oxide (NO) were measured. Pulmonary superoxide dismutase (SOD), glutathione peroxidase (GPx) activity, glutathione (GSH), malondialdehyde (MDA) contents, and myeloperoxidase (MPO) activity were also determined. The expression of glucocorticoid receptor (GR) level was detected by Western blotting. Pretreatment with escin could decrease the mortality rate, attenuate lung injury resulted from LPS, down-regulate the level of the inflammation mediators, including NO, TNF-α, and IL-1β, enhance the endogenous antioxidant capacity, and up-regulating the GR expression in lung. The results suggest that escin may have potent protective effect on the LPS-induced ALI by inhibiting of the inflammatory response, and its mechanism involves in up-regulating the GR and enhancing the endogenous antioxidant capacity.
Department of Pharmacology, School of Pharmacy, Yantai University, Yantai, Shandong, PR China.
Wenyu
W
Xin
Leiming
L
Zhang
Huaying
H
Fan
Na
N
Jiang
Tian
T
Wang
Fenghua
F
Fu
D055371:Acute Lung Injury / Q000139:chemically induced / Q000201:enzymology / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000627:therapeutic use*; D000975:Antioxidants / Q000378:metabolism; D015153:Blotting, Western; D004928:Escin / Q000008:administration & dosage / Q000627:therapeutic use*; D005979:Glutathione Peroxidase / Q000378:metabolism; D053583:Interleukin-1beta / Q000276:immunology; D008070:Lipopolysaccharides / Q000633:toxicity*; D008168:Lung / Q000187:drug effects* / Q000201:enzymology / Q000276:immunology / Q000473:pathology; D008297:Male; D051379:Mice; D009569:Nitric Oxide / Q000096:biosynthesis; D009195:Peroxidase / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D016019:Survival Analysis; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000975:Antioxidants; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; C482199:lipopolysaccharide, E coli O55-B5; D009569:Nitric Oxide; D004928:Escin; D009195:Peroxidase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase