Diammonium Glycyrrhizinate Promotes Aquaporin-5 in LPS-induced Acute Lung Injury via Inactivation of NF-κB
Abstract
To determine the therapeutic value and associated mechanism of diammonium glycyrrhizinate (DG) on the expression of AQP-5 in lipapolysacchairides (LPS)-induced acute lung injury in mice. Methods Thirty male BALB/c mice were randomly divided into three groups equally: Control, LPS+DG and LPS. HE staining and lung injury score system were used to evaluate the pathological changes in the lung tissues. Wet to dry ratio (W/D) was used to measure the degree of lung edema. RT-PCR and Western blot were obtained to measure AQP-5 expression. Total NF-κB p65 and phospho-NF-κB p65 (p-NF-κB p65) were evaluated by Western blot. Results After 3 days of LPS intratracheal injection, severe pathological changes, increased W/D, down-regulated AQP-5 expression and increased p-NF-κB p65/total NF-κB p65 were observed. Compared with mice in the LPS group, mice in the LPS+DG group had more significantly ameliorated pathological changes and increased W/D, up-regulated AQP-5 expression, and reduced p-NF-κB p65/total NF-κB p65. Conclusion DG up-regulates AQP-5 in vivo, possibly resulting from inactivation of NF-κB.
Keywords: Diammonium glycyrrhizinate (DG), Acute lung injury (ALI), Aquaporin-5 (AQP-5)
Full Text:
PDFReferences
Ware LB, Matthay MA. The acute respiratory distress syndrome. N Engl J Med, 2000,342( 18): 1334-1349.
Wheeler AP, Bernard OR. Acute lung injury and the acute respiratory distress syndrome:a clinical review. Lancet, 2007, 369(9572):1553-1564.
Li J, Xu M, Fan Q. et al. Tanshinone H A ameliorates seawater exposure-induced lung injury by inhibiting aquaporins (AQP) 1 and AQP5 expression in lung. Respir Physiol Neurobiol. 2011, 176( 1-2);39-49.
Feng С, Wang Н, Yao С, et al. Diammoniumglycyrrhizinate, a component of traditional Chinese medicine Gan-Cao, prevents murine T-cell-mediated fulminant hepatitis in IL-10- and IL-6- dependent manners. Intlmmunopharmacol, 2007 ; 7( 10): 1292- 1298.
Song HY, Mao ZM, Yang LL, et al. Dangfeiliganning capsules attenuate the susceptibility of rat nonalcoholic fatty liver to carbon tetrachloride toxicity. J Tradit Chin Med.2011; 31(4);327-333.
Yao C, Purwanti N, Karabasil MR, et al. Potential down- regulation of sali'ary gland AQP5 by LPS via cross-coupling of NF-kappaB and p-c-Jun/c-Fos. Am J Pathol, 2010; 177 ( 2); 724-734.
Zhu T, Wang DX, Zhang W, et al. Andrographolide protects against LPS-induced acute lung injury by inactivation of NF- KB. PLoS One,2013;8(2) ;e56407.
Zhu T, Zhang W. Wang I)X. Insulin up-regulates epithelial sodium channel in LPS-induced acute lung injury model in rats by SGK1 activation. Injury,2012;43(8): 1277-1283.
Martin GS, Brigham KL. Fluid flux and clearance in acute lung injury. Compr Physiol,2012;2(4):2471-2480.
Wang L, Taneja R, Wang W. et al. Human alveolar epithelial cells attenuate pulmonary microvascular endothelial cell permeability under septic conditions. PLoS One, 2013; 8 ( 2 ); e55311.
Eckle T, Hughes К, Ehrentraut H, et al. Crosstalk between the equilibrative nucleoside transporter ENT2 and alveolar Adora2b adenosine receptors dampens acute lung injury. FASEB J,2013; 27(8): 3078-3089.
Eckle T, Brodsky K, Bonney M, et al. HIF1A reduces acute lung injury by optimizing carbohydrate metabolism in the alveolar epithelium. PLoS Biol,2013; 11 (9);el001665.
Zeyed YF, Bastarache JA, Matthay MA, et al. The severity of shock is associated with impaired rates of net alveolar fluid clearance in clinical acute lung injury. Am J Physiol Lung Cell Mol Physiol, 2012; 303 (6): L550-555.
BengaG. On the definition, nomenclature and classification of water channel proteins ( aquaporins and relatives ). Mol Aspects Med,2012;33(5-6):514-517.
Loitto VM, Karlsson T, Magnusson KE. Water flux in cell motility: expanding the mechanisms of membrane protrusion. Cell Motil Cytoskeleton,2009;66(5):237-247.
Ma T, Fukuda N, Song Y, et al. Lung fluid transport in aquaporin-5 knockout mice. J Clin Invest, 2000; 105 ( 1 ); 93- 100.
Refbacks
- There are currently no refbacks.
