| Objective: After replication hemorrhagic shock rat model with ALI,toobserve the expression of PPAR-β in ALI lung tissue; PPARβ activator(GW0742),antagonist (GSK0660),GW0742and GSK0660,combined ratmodel of ALI intervention,observationALI lung tissue of rats withhemorrhagic shock PPARβ expression of PPARβ in ALI protective effectand mechanism of the development process.Methods: A copy of hemorrhagic shock in rats model of ALI, completelyrandom principle120SD rats were divided into five groups, sham operationgroup (group A), hemorrhagic shock induced acute lung injury model group(group B),GSK0660group(Cgroup),GW0742group (D) and the combinationgroup (E group).Each group is divided into1h,2h,4h,6h four time points,each phase point6mice. Specific methods of operation A group actionvenipuncture,do not have the hemorrhagic shock model of ALI,intravenousinjection of10%DMSO3ml/kg B group received intravenous injection of10%DMSO3ml/kg30min after injection of saline2.5ml/kg copied afterhemorrhagic shock rat model of ALI;and group C first intravenousGSK06603mg/Kg in rats,30min after injection of saline2.5ml/kg, copythe model of hemorrhagic shock ALI.Group D first intravenousGW07423mg/Kg in rats,30min after injection of saline2.5ml/kg copy ALImodel of hemorrhagic shock. Group E first intravenous injection in ratsGSK0660+GW0742, between injection time separated15min,30min afterinjection of saline2.5ml/kg copy ALI model of hemorrhagic shock.Observed and recorded at1,2,4,6hours lung tissue determination ofPPARβ receptor expression parallel pathological examination, lungneutrophil infiltration in the lung wet and dry weight ratio coefficient and bronchoalveolar lavage fluid (BALF) total protein as an indicator of thedegree of detection of lung injury. Detection of lung tissue antioxidantenzymes SOD, CAT and gsh-px activity8-iso-PGF2alpha oxidationproduct content to evaluate the oxidative stress state to assess bodyoxidative stress state.Then give PPARβ receptor antagonist pretreatment,observe animal indicators of hemorrhagic shock due to acute lung injury,and to investigate the inflammatory factors, oxidation and antioxidantsystem of apoptosis effect.Results:1. Uncontrolled hemorrhagic shock injuries group rats antioxidant enzymesSOD, CAT and gsh-px activity was significantly higher in the control group(P <0.05).2. GW0742make ALI in the lung tissue antioxidant enzymes SOD, CAT andgsh-px activity in each phase is simply uncontrolled hemorrhagic shockinjury group has different rate reduce, in2h,4h increased mostsignificantly (P <0.05).3. Used alone GW0742rats can improve PaO2, W/D ratio of lung tissue,lung tissue pathology score, lung tissue SOD, CAT and gsh-px activity (P <0.05) and reduce the content of8-iso-PGF2alpha; Using antagonistsGSK0660makes the function reduce (P <0.05).Conclusion:1, ALI uncontrolled hemorrhagic shock in rats model of lung tissue SOD,CAT and gsh-px activity was significantly elevated, prompt uncontrolledhemorrhagic shock in acute oxidative stress state.2. GW0742could significantly increase ALI rats lung tissue SOD, CAT andgsh-px activity, reduce oxidation product content of8-iso-PGF2alpha.3. Speculation GW0742through could inhibit the TNF alpha gene andprotein expression, reduce the lung tissue SOD activity of ALI some degreeof protective lung tissue, reduce ALI inflammation of lung tissue, improvethe PaO2, may be by preventing the nf-kappa B activation play a role. |