河北医药
河北醫藥
하북의약
HEBEI MEDICAL JOURNAL
2013年
23期
3540-3542
,共3页
杂种犬%急性肺动脉高压%炎性反应%MCP-1
雜種犬%急性肺動脈高壓%炎性反應%MCP-1
잡충견%급성폐동맥고압%염성반응%MCP-1
mongrel dogs%acute pulmonary hypertension%inflammatory response%MCP-1
目的:探讨硫酸镁对急性肺栓塞肺动脉高压的影响及其抗炎机制。方法18只杂种犬,随机分为空白组、对照组及硫酸镁2.0 mm/kg组(MgSO42.0组),每组6只。其中空白组不给于任何处理,对照组只给予处理造成急性肺动脉高压,MgSO42.0组造成急性肺动脉高压稳定30 min后,以2.0 mm/kg 10 min内静脉滴注给予硫酸镁;肺动脉、股动脉插管检测平均肺动脉压( MPAP )、体循环平均动脉压(MAP),应用酶联免疫吸附以及放免法分别测定血清中白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α), western blot 测定肺组织中MCP-1蛋白表达。结果对照组MPAP较空白组显著升高,MgSO42.0组MPAP较对照组显著下降( P <0.05或<0.01);对照组MAP较空白组显著下降,MgSO42.0组MAP较对照组显著升高( P <0.05或<0.01);对照组血清中TNF-α以及IL-6空白组显著升高,MgSO42.0组TNF-α以及IL-6较对照组显著下降( P <0.05或<0.01);对照组MCP-1蛋白表达较空白组显著升高,MgSO42.0组MCP-1蛋白表达较对照组显著下降( P <0.05或<0.01)。结论硫酸镁可显著降低肺动脉高压,这可能与其抑制肺组织MCP-1表达,降低TNF-α以及IL-6,从而抑制炎性反应增强有关。
目的:探討硫痠鎂對急性肺栓塞肺動脈高壓的影響及其抗炎機製。方法18隻雜種犬,隨機分為空白組、對照組及硫痠鎂2.0 mm/kg組(MgSO42.0組),每組6隻。其中空白組不給于任何處理,對照組隻給予處理造成急性肺動脈高壓,MgSO42.0組造成急性肺動脈高壓穩定30 min後,以2.0 mm/kg 10 min內靜脈滴註給予硫痠鎂;肺動脈、股動脈插管檢測平均肺動脈壓( MPAP )、體循環平均動脈壓(MAP),應用酶聯免疫吸附以及放免法分彆測定血清中白細胞介素-6(IL-6)和腫瘤壞死因子-α(TNF-α), western blot 測定肺組織中MCP-1蛋白錶達。結果對照組MPAP較空白組顯著升高,MgSO42.0組MPAP較對照組顯著下降( P <0.05或<0.01);對照組MAP較空白組顯著下降,MgSO42.0組MAP較對照組顯著升高( P <0.05或<0.01);對照組血清中TNF-α以及IL-6空白組顯著升高,MgSO42.0組TNF-α以及IL-6較對照組顯著下降( P <0.05或<0.01);對照組MCP-1蛋白錶達較空白組顯著升高,MgSO42.0組MCP-1蛋白錶達較對照組顯著下降( P <0.05或<0.01)。結論硫痠鎂可顯著降低肺動脈高壓,這可能與其抑製肺組織MCP-1錶達,降低TNF-α以及IL-6,從而抑製炎性反應增彊有關。
목적:탐토류산미대급성폐전새폐동맥고압적영향급기항염궤제。방법18지잡충견,수궤분위공백조、대조조급류산미2.0 mm/kg조(MgSO42.0조),매조6지。기중공백조불급우임하처리,대조조지급여처리조성급성폐동맥고압,MgSO42.0조조성급성폐동맥고압은정30 min후,이2.0 mm/kg 10 min내정맥적주급여류산미;폐동맥、고동맥삽관검측평균폐동맥압( MPAP )、체순배평균동맥압(MAP),응용매련면역흡부이급방면법분별측정혈청중백세포개소-6(IL-6)화종류배사인자-α(TNF-α), western blot 측정폐조직중MCP-1단백표체。결과대조조MPAP교공백조현저승고,MgSO42.0조MPAP교대조조현저하강( P <0.05혹<0.01);대조조MAP교공백조현저하강,MgSO42.0조MAP교대조조현저승고( P <0.05혹<0.01);대조조혈청중TNF-α이급IL-6공백조현저승고,MgSO42.0조TNF-α이급IL-6교대조조현저하강( P <0.05혹<0.01);대조조MCP-1단백표체교공백조현저승고,MgSO42.0조MCP-1단백표체교대조조현저하강( P <0.05혹<0.01)。결론류산미가현저강저폐동맥고압,저가능여기억제폐조직MCP-1표체,강저TNF-α이급IL-6,종이억제염성반응증강유관。
Objective To investigate the effect of magnesium sulfate on acute pulmonary hypertension and its anti-inflammatory mechanism in mongrel dogs .Methods 18 mongrel dogs were randomly divided into three groups:blank group,control group and magnesium sulfate group (2.0mm/kg),with 6 dogs in each group.The dogs in blank group were not given any treatment ,the dogs in control group were operated to induce acute pulmonary hypertension,and the dogs in magnesium sulfate group were given magnesium sulfate 2.0mm/kg by intravenous infusion for 10 minutes after the animal models with acute pulmonary hypertension were established .The mean pulmonary artery pressure ( MPAP) and circulation mean arterial pressure ( MAP) were detected by pulmonary artery and femoral artery cannulation , IL-6 and TNF-αlevels in serum were detected by enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay,respectively,and MCP-1 protein expression was determined by Western blot .Results The MPAP in control group was significantly higher than that in blank group;however MPAP in magnesium sulfate group was significantly lower than that in control group ( P <0.05 or P <0.01).The MAP in control group was significantly lower than that in blank group ,however,MAP in magnesium sulfate group was significantly higher than that in control group ( P <0.05 or P <0.01).The serum levels of TNF-αand IL-6 in control group were significantly higher that those in blank group , however , which in magnesium sulfate group were significantly lower than those in control group ( P <0.05 or P <0.01).The MCP-1 protein expression levels in control group were significantly higher than those in blank group ,however ,which in magnesium sulfate group was significantly lower than those in control group ( P <0.05 or P <0.01).Conclusion Magnesium sulfate can significantly reduce acute pulmonary hypertension ,which may be related to its effects of inhibiting the expression of MCP-1 in lung tissue,decrease TNF-αand IL-6 levels so as to inhibit inflammatory response .