羟乙基淀粉（130/0.4）对重症急性胰腺炎大鼠脑毛细血管渗漏的影响
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摘要
目的探讨羟乙基淀粉对SAP大鼠脑毛细血管渗漏的影响。
方法将雄性SD大鼠50只按完全随机法分为假手术(sham operation, SO)组、重症急性胰腺炎(severe acute pancreatitis,SAP)组、羟乙基淀粉(hydroxyethyl starch,HES)治疗组,每组又分为6h、24h两个亚组,其中24hSAP组10只,余亚组各8只。以胰胆管逆行注射5%牛磺胆酸钠建立SAP模型。观察6h、24h后各组测血清TNF-α以及胰腺、脑组织病理,干湿重法检测脑含水率,RT-PCR检测脑组织AQP4mRNA表达,免疫组化检测脑组织AQP4蛋白表达。
结果SO组、SAP组、HES治疗组6h血清TNF-α分别为(35.84±11.91)pg/ml、(97.14±6.70)pg/ml、(78.29±4.77)pg/ml,24h血清TNF-α分别为(38.58±12.22)pg/ml、(148.49±24.77)pg/ml、(112.50±7.11)pg/ml,组间差异均显著(P<0.05);6h脑组织含水率分别为(76.98±0.57)%、(79.72±0.62)%、(78.13±0.25)%,24 h脑组织含水率分别为(77.30±0.83)%、(80.44±0.54)%、(78.59±0.42)%,组间差异均显著(P<0.05);6h脑组织AQP4mRNA表达分别为0.5083±0.0466、0.7735±0.0243、0.6767±0.0255,24 h脑组织AQP4mRNA表达分别为0.5480±0.0488、0.8142±0.0168、0.7181±0.0188,组间差异均显著(P<0.05);6h脑组织AQP4蛋白表达分别为3.25±1.04、6.88±1.89、4.63±2.07,24 h脑组织AQP4蛋白表达分别为3.50±0.93、7.50±1.60、5.63±1.69,组间差异均显著(P<0.05)。SAP6h、24h两亚组血清TNF-α、脑组织含水率、脑组织AQP4mRNA、脑组织AQP4蛋白表达均较SO组显著增高(P<0.05),HES治疗组6h、24h两亚组血清TNF-α、脑组织含水率、脑组织AQP4mRNA、脑组织AQP4蛋白表达均较SAP组显著降低。结论羟乙基淀粉(130/0.4)可能通过抑制炎症因子TNF-α水平,间接下
调脑组织AQP4表达,致脑毛细血管渗漏作用减弱。羟乙基淀粉(130/0.4)对改善SAP脑毛细血管渗漏有一定的意义。
Objective To investigate the effect of hydroxyethyl starch on brain capillary permeability in rats with severe acute pancreatitis.Methods 50 male Sprague-Dawley rats were randomly divided into sham operation(SO) group, severe acute pancreatitis(SAP)group, hydroxyethyl starch(HES) treated group.Each group was divided into two subgroups as 6h and 24h,with 8 rats each subgroup except for 10 rates in 24h SAP group.Model was induced by injecting 5% sodium taurocholate into pancreaticobiliary.Serum TNF-α,the brain water content,pathological changes of brain and pancreas were measured and the expression of AQP4 was determined by RT-PCR plus immunohistochemistry 6h and 24h after induction.Result The levels of serum TNF-αin sham operation(SO) group,SAP group, hydroxyethyl starch(HES) treated group were (35.84±11.91)pg/ml、(97.14±6.70)pg/ml、(78.29±4.77)pg/ml in 6h,they were (38.58±12.22)pg/ml、(148.49±24.77 ) pg/ml、( 112.50±7.11 ) pg/ml in 24h,with significant difference(P<0.05). The water content were (76.98±0.57)%、(79.72±0.62)%、(78.13±0.25)% in 6h,they were (77.30±0.83)%、(80.44±0.54)%、(78.59±0.42)% in 24h, with significant difference(P<0.05). The expression of AQP4 mRNA were 0.5083±0.0466、0.7735±0.0243、0.6767±0.0255 in 6h,they were 0.5480±0.0488、0.8142±0.0168、0.7181±0.0188 in 24h, with significant difference(P<0.05). The expression of AQP4 proteins were 3.25±1.04、6.88±1.89、4.63±2.07 in 6h,they were 3.50±0.93、7.50±1.60、5.63±1.69 in 24h,with significant difference(P<0.05).Both in 6h and 24h,compared with sham operation group,the levels of serum TNF-α,the water content and the expression of AQP4 mRNA and proteins in SAP group were significantly increased(P<0.05).Compared with SAP group,the levels of serum TNF-α,the water content and the expression of AQP4 mRNA and proteins decreased obviously in HES treated group(P<0.05).Conclusions HES may inhibit the inflammatory factor--TNF-α,indirectly down-regulate the expression of AQP4,which may play an important role to decrease the effect of brain capillary permeability in SAP.HES may alleviate the brain capillary permeability in SAP.
方法将雄性SD大鼠50只按完全随机法分为假手术(sham operation, SO)组、重症急性胰腺炎(severe acute pancreatitis,SAP)组、羟乙基淀粉(hydroxyethyl starch,HES)治疗组,每组又分为6h、24h两个亚组,其中24hSAP组10只,余亚组各8只。以胰胆管逆行注射5%牛磺胆酸钠建立SAP模型。观察6h、24h后各组测血清TNF-α以及胰腺、脑组织病理,干湿重法检测脑含水率,RT-PCR检测脑组织AQP4mRNA表达,免疫组化检测脑组织AQP4蛋白表达。
结果SO组、SAP组、HES治疗组6h血清TNF-α分别为(35.84±11.91)pg/ml、(97.14±6.70)pg/ml、(78.29±4.77)pg/ml,24h血清TNF-α分别为(38.58±12.22)pg/ml、(148.49±24.77)pg/ml、(112.50±7.11)pg/ml,组间差异均显著(P<0.05);6h脑组织含水率分别为(76.98±0.57)%、(79.72±0.62)%、(78.13±0.25)%,24 h脑组织含水率分别为(77.30±0.83)%、(80.44±0.54)%、(78.59±0.42)%,组间差异均显著(P<0.05);6h脑组织AQP4mRNA表达分别为0.5083±0.0466、0.7735±0.0243、0.6767±0.0255,24 h脑组织AQP4mRNA表达分别为0.5480±0.0488、0.8142±0.0168、0.7181±0.0188,组间差异均显著(P<0.05);6h脑组织AQP4蛋白表达分别为3.25±1.04、6.88±1.89、4.63±2.07,24 h脑组织AQP4蛋白表达分别为3.50±0.93、7.50±1.60、5.63±1.69,组间差异均显著(P<0.05)。SAP6h、24h两亚组血清TNF-α、脑组织含水率、脑组织AQP4mRNA、脑组织AQP4蛋白表达均较SO组显著增高(P<0.05),HES治疗组6h、24h两亚组血清TNF-α、脑组织含水率、脑组织AQP4mRNA、脑组织AQP4蛋白表达均较SAP组显著降低。结论羟乙基淀粉(130/0.4)可能通过抑制炎症因子TNF-α水平,间接下
调脑组织AQP4表达,致脑毛细血管渗漏作用减弱。羟乙基淀粉(130/0.4)对改善SAP脑毛细血管渗漏有一定的意义。
Objective To investigate the effect of hydroxyethyl starch on brain capillary permeability in rats with severe acute pancreatitis.Methods 50 male Sprague-Dawley rats were randomly divided into sham operation(SO) group, severe acute pancreatitis(SAP)group, hydroxyethyl starch(HES) treated group.Each group was divided into two subgroups as 6h and 24h,with 8 rats each subgroup except for 10 rates in 24h SAP group.Model was induced by injecting 5% sodium taurocholate into pancreaticobiliary.Serum TNF-α,the brain water content,pathological changes of brain and pancreas were measured and the expression of AQP4 was determined by RT-PCR plus immunohistochemistry 6h and 24h after induction.Result The levels of serum TNF-αin sham operation(SO) group,SAP group, hydroxyethyl starch(HES) treated group were (35.84±11.91)pg/ml、(97.14±6.70)pg/ml、(78.29±4.77)pg/ml in 6h,they were (38.58±12.22)pg/ml、(148.49±24.77 ) pg/ml、( 112.50±7.11 ) pg/ml in 24h,with significant difference(P<0.05). The water content were (76.98±0.57)%、(79.72±0.62)%、(78.13±0.25)% in 6h,they were (77.30±0.83)%、(80.44±0.54)%、(78.59±0.42)% in 24h, with significant difference(P<0.05). The expression of AQP4 mRNA were 0.5083±0.0466、0.7735±0.0243、0.6767±0.0255 in 6h,they were 0.5480±0.0488、0.8142±0.0168、0.7181±0.0188 in 24h, with significant difference(P<0.05). The expression of AQP4 proteins were 3.25±1.04、6.88±1.89、4.63±2.07 in 6h,they were 3.50±0.93、7.50±1.60、5.63±1.69 in 24h,with significant difference(P<0.05).Both in 6h and 24h,compared with sham operation group,the levels of serum TNF-α,the water content and the expression of AQP4 mRNA and proteins in SAP group were significantly increased(P<0.05).Compared with SAP group,the levels of serum TNF-α,the water content and the expression of AQP4 mRNA and proteins decreased obviously in HES treated group(P<0.05).Conclusions HES may inhibit the inflammatory factor--TNF-α,indirectly down-regulate the expression of AQP4,which may play an important role to decrease the effect of brain capillary permeability in SAP.HES may alleviate the brain capillary permeability in SAP.
引文
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[3]Pascual JL,Ferri LE,Chaudhury P,et a1.Hemorrhagic shock resuscitation with a low molecular weight starch reduces neutrophil-endothelial interactions and vessel leakage in vivo.Surg Infect(Larchmt),2001,2(4):275-287;discussion 287-288.
[4]Hoffmann JN,Vollmar B,Laschke MW,et a1.Hydroxyethyl starch(130 kD),but not crystalloid volume support,improves microcirculation during normotensive endotoxemia.Anesthesiology,2002,97(2):460-470.
[5]Tian J,Lin X,Guan R,et a1.The efects of hydroxyethyl starch on lung capillary permeability in endotoxic rats and possible mechanisms. Anesth Analg,2004,98(3):768-774.
[6]Tian J,Lin X,Zhou W,et a1.Hydroxyethyl starch inhibits NF-kappaB activation and prevents the expression of inflammatory mediators in endotoxic rats.Ann Clin Lab Sci,2003,33(4):451-458.
[7]Boldt J,Ducke M,Kumle B,et a1.Influence of diferent volume replacement strategies on inflammation and endothelial activation in the elderly undergoing major abdominal surgery.Intensive Care Med.2004,30(3):416-422.
[8]Lang K,Suttner S,Boldt J,et a1.Volume replacement with HES 130/0.4 may reduce the inflammatory response in patients undergoing major abdominal surgery.Can J Anaesth,2003,50(10):1009-1016.
[9]Solenov E,Watanabe H,Mamnley GT,et a1.Sevenfold-reduced osmotic water permeability in primary astrocyte cultures from AQP-4-deficient mice,measured by a fluorescence quenching method.Am J Physiol Cell Physiol,2004,286(2):426-432.
[10]Nicchia GP,Frigeri A,Liuzzi GM,et a1.Inhibition of aquaporin-4expression in astrocytes by RNAi determines alterations in cell morphology,growth,and water transport and induces changes in ischemia related genes.FASEB J,2003,17(11):l508-1510.
[11]Connors NC,Adams ME,Froehner SC,et a1.The potassium channel Kit4.1 associates with the dystrophin-glycoprotein complex via alpha-syntrophin in glia.J Biol Chem,2004,279(27):28387-28392.
[12]杨波,黄鹤光,陈大良,等.逆行性胰胆管注射法制作重症急性胰腺炎大鼠模型.福建医科大学学报,2002,36(1):71-72.
[13]中华医学会外科学分会胰腺外科学组.重症急性胰腺炎诊治指南.中华外科杂志,2007,45:727-729.
[14]Norman J.The role of cytokines the pathogenesis of acute pancreatitis [J].Am J Surg,1998,175(1):76-83.
[15]Yang YL,Li JP,LiKZ,et al.Tumor necrosis factor alphs antibody prevents brain damage of rats with acute necrotizing pancreatitis. World J Gastroenterol,2O04,10(19):2898-2900.
[16]Farkas G,Marton J,Nagy Z,et al.Experimental acute pancreatitis results in increased blood-brain barrier permeability in the rat:a potential role for tumor necrosis factor and interleukin 6. Neurosci lett,1998,242(3):147-150.
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