胆红素对内毒素致急性肺损伤大鼠水通道蛋白1、5表达的影响
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摘要
目的探讨胆红素对脂多糖所致急性肺损伤大鼠的水通道蛋白1、5是否存在调节作用,探讨其保护作用机制。方法雄性Wistar大鼠18只,随机分为生理盐水对照组(C组)、脂多糖模型组(L组)和胆红素预处理组(B组),每组各6只。每组于造模后4 h处死大鼠。测定每组肺湿/干重比值,ELISA法测血清中IL-8含量,肺组织中cAMP含量,免疫组化法测定每组水通道蛋白1、5的表达变化,观察各组肺组织病理改变。结果与模型组(L组)比较,胆红素干预组(B组)的W/D值下降,IL-8含量明显降低,cAMP含量表达上升(P<0.05),水通道蛋白1、5表达增强(P<0.05),肺水肿病理改变明显减轻。结论胆红素可能是通过cAMP信号途径调节水通道蛋白1、5表达改善水代谢,减轻肺水肿状态,从而对急性肺损伤具有保护作用。
Objective To discuss whether the bilirubin had the regulating effect on aquaporin-1 and aquaporin-5 of rats injured by the acute lung injury caused by the lipopolysaccharide and the protective mechanism.Methods Select ed 18 male rats of wistar,which shall be divided randomLy into control group for normal saline(group C),model group for lipopolysaccharide(group L) and preconditioning group for bilirubin(group B) with 6 rats respectively.All rats shall be killed after 4 h molding.The wet-to-dry weight ratio of the lung per group was measured,the content of IL-8 in serum and the content of cAMP in lung tissue by ELISA method.The expression change of aquaporin-1 and aqua porin-5 per group was examined by immunohistochemical method and the changes of lung tissue per group was patho logically observed.Results Compared with the model group(group L),the ratio of wet to dry lung weight and the content of IL-8 was significantly reduced in preconditioning group for bilirubin(group B)(P < 0.05).The content of cAMP and the expression of protein of aquaporin-1 and aquaporin-5 had a increased significantly in group B(P < 0.05),and pathologic change of pulmonary edema was reduced significantly.Conclusion The bilirubin may improved the water metabolism and reduced the pulmonary edema state by regulating the aquaporin-1 and aquaporin-5 expressions to had a protective effect to the acute lung injury.
Objective To discuss whether the bilirubin had the regulating effect on aquaporin-1 and aquaporin-5 of rats injured by the acute lung injury caused by the lipopolysaccharide and the protective mechanism.Methods Select ed 18 male rats of wistar,which shall be divided randomLy into control group for normal saline(group C),model group for lipopolysaccharide(group L) and preconditioning group for bilirubin(group B) with 6 rats respectively.All rats shall be killed after 4 h molding.The wet-to-dry weight ratio of the lung per group was measured,the content of IL-8 in serum and the content of cAMP in lung tissue by ELISA method.The expression change of aquaporin-1 and aqua porin-5 per group was examined by immunohistochemical method and the changes of lung tissue per group was patho logically observed.Results Compared with the model group(group L),the ratio of wet to dry lung weight and the content of IL-8 was significantly reduced in preconditioning group for bilirubin(group B)(P < 0.05).The content of cAMP and the expression of protein of aquaporin-1 and aquaporin-5 had a increased significantly in group B(P < 0.05),and pathologic change of pulmonary edema was reduced significantly.Conclusion The bilirubin may improved the water metabolism and reduced the pulmonary edema state by regulating the aquaporin-1 and aquaporin-5 expressions to had a protective effect to the acute lung injury.
引文
[1]许银姬,陈远彬,王丽丽,等.青天葵对内毒素致急性肺损伤大鼠肺水通道蛋白1和5表达的影响[J].中国中西医结合杂志,2010,30(8):861-866.
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[7]Chenjuan Yao,Nunuk Purwanti,Mileva Ratko Karabasil,et al.Poten-tial down-regulation of salivary gland AQP5by LPS via cross-cou-pling of NF-κB and p-c-Jun/c-Fos[J].Am J Pathol,2010,177(2):724-734.
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[10]Towse JE,Harrod KS,Krane CM,et al.Decreased expression of AQP1and AQP5in mouse lung after acute viral infection[J].Am JRespir Cell Mol Biol,2000,22(1):34-44.
[11]Jiao GY,Li ER,Yu RJ.Decreased expression of AQP-1andAQP-5 in acute injured lung in rats[J].Chin Med J,2002,115(7):963-967.
[12]Li J,Xu M,Fan Q,et al.Tanshinone IIA ameliorates seawater expo-sure-induced lung injury by inhibiting aquaporins(AQP)1and AQP5 expression in lung[J].Respir Physiol Neurobiol,2011,176(1-2):39-49.
[13]路炜,漆洪波.水通道蛋白的研究进展[J].国外医学:妇幼保健分册,2005,16(1):42-44.
[14]何琳,李涛平,朱丽华.油酸肺损伤时肺泡内液体清除和肺泡Ⅱ型细胞内cAMP、cGMP水平的变化[J].南方医科大学学报,2008,28(4):513-514.
[15]Lang D,Reuter S,Buzescu T,et al.Heme-induced heme oxygenase-1(HO-1)in human monocytes inhibits apoptosis despite caspase-3 upregulation[J].Int Immunol,2005,17(2):155-165.
[16]李建强,高晓玲,刘卓拉,等.胆红素对抗脂多糖诱导致大鼠急性肺损伤的实验研究[J].中国病理生理杂志,2005,21(4):780-783.
[17]李建强,高晓玲,刘卓拉,等.胆红素对急性肺损伤大鼠肺血管内皮细胞核因子-κB,细胞间粘附分子1表达的影响[J].中国组织化学与细胞化学杂志,2004,13(1):1-4.
[18]任文霞,弓清梅,赵鹰,等.胆红素对大鼠急性肺损伤形成过程中氧自由基以及caspase-3表达的影响[J].中国病理生理杂志,2007,23(2):293-296.
[2]Insang Hwang,Seung-II Jung,Eu-Chang Hwang,et al.Expression and localization of aquaporins in benign prostate hyperplasia and prostate cancer[J].Chonnam Med J,2012,48(3):174-178.
[3]Verkman AS,Matthay MA,Song Y.Aquaporin water channels and lung physiology[J].Am J Physiol Lung Cell Mol Physiol,2000,278(5):L867-L879.
[4]李建强,高晓玲,刘卓拉,等.胆红素对抗脂多糖诱导致大鼠急性肺损伤的实验研究[J].中国病理生理杂志,2005,21(4):780-783.
[5]Rudolf Lucas,Supriya Sridhar,Ferenc G.Rick,et al.Agonist of growth hormone-releasing hormone reduces pneumolysin-induced pulmonary permeability edema[J].Proc Natl Acad Sci USA,2012,109(6):2084-2089.
[6]李珊珊,赵光瑜,王忠慧.水通道蛋白在急性肺损伤中的表达及调节[J].河北医药,2011,33(16):2498-2500.
[7]Chenjuan Yao,Nunuk Purwanti,Mileva Ratko Karabasil,et al.Poten-tial down-regulation of salivary gland AQP5by LPS via cross-cou-pling of NF-κB and p-c-Jun/c-Fos[J].Am J Pathol,2010,177(2):724-734.
[8]郭亮,张端莲.水通道蛋白与急性肺损伤[J].华南国防医学杂志,2009,23(1):81-83.
[9]赵建军,张建勇,陈玲.内毒素致急性肺损伤大鼠水通道蛋白1、5表达的影响[J].中国药师,2012,15(1):41-44.
[10]Towse JE,Harrod KS,Krane CM,et al.Decreased expression of AQP1and AQP5in mouse lung after acute viral infection[J].Am JRespir Cell Mol Biol,2000,22(1):34-44.
[11]Jiao GY,Li ER,Yu RJ.Decreased expression of AQP-1andAQP-5 in acute injured lung in rats[J].Chin Med J,2002,115(7):963-967.
[12]Li J,Xu M,Fan Q,et al.Tanshinone IIA ameliorates seawater expo-sure-induced lung injury by inhibiting aquaporins(AQP)1and AQP5 expression in lung[J].Respir Physiol Neurobiol,2011,176(1-2):39-49.
[13]路炜,漆洪波.水通道蛋白的研究进展[J].国外医学:妇幼保健分册,2005,16(1):42-44.
[14]何琳,李涛平,朱丽华.油酸肺损伤时肺泡内液体清除和肺泡Ⅱ型细胞内cAMP、cGMP水平的变化[J].南方医科大学学报,2008,28(4):513-514.
[15]Lang D,Reuter S,Buzescu T,et al.Heme-induced heme oxygenase-1(HO-1)in human monocytes inhibits apoptosis despite caspase-3 upregulation[J].Int Immunol,2005,17(2):155-165.
[16]李建强,高晓玲,刘卓拉,等.胆红素对抗脂多糖诱导致大鼠急性肺损伤的实验研究[J].中国病理生理杂志,2005,21(4):780-783.
[17]李建强,高晓玲,刘卓拉,等.胆红素对急性肺损伤大鼠肺血管内皮细胞核因子-κB,细胞间粘附分子1表达的影响[J].中国组织化学与细胞化学杂志,2004,13(1):1-4.
[18]任文霞,弓清梅,赵鹰,等.胆红素对大鼠急性肺损伤形成过程中氧自由基以及caspase-3表达的影响[J].中国病理生理杂志,2007,23(2):293-296.