The Protective Effect And Mechanism Of Astragalus Polysaccharide On Liver Injury In The State Of Brain Death

Objective: The purpose of this experiment is to copy a progressive intracranialpressure with brain death model, observe the vital signs in the process of induction ofbrain death and brain death to cardiac death. Investigate the damage of the liver in thestate of brain death and its mechanism. Explore the Astragalus polysaccharide (APS)on the liver in the rabbit brain death to cardiac death process and its possiblemechanism.This experiment is divided into two parts.The first part: Copy progressive intracranial pressure with brain death model toobserve the vital signs in the process of induction of brain death and brain death tocardiac death.Methods: Using healthy adult New Zealand rabbits were12rats of either sex, weight(2.8±0.3) Kg.The rabbits were randomly divided into sham operation group (groupC), brain death4h group (group B1) and brain-death of8h groups (B2group)(n=4).Group C tracheal intubation, the femoral artery and vein catheterization; drillingintracranial set Foley balloon catheter, but not pressurized, anesthesia8h. B1and B2pressure copy of brain death were kept after4h,8h, the monitoring of brain death toestablish the course of MAP, HR, the RR changes and stop the rescue, MAP, HRvalue, record the stop rescue to cardiac death.Part Ⅱ: Brain death status of liver function and morphology and its mechanism, theprotective effects of Astragalus polysaccharides on the brain death of the rabbit liver.Methods: Using healthy adult New Zealand rabbits24only, either male or female,body weight (2.8±0.3) Kg, and randomly divided into three groups (n=8): ie, shamsurgery group (C group), brain death group (B group), astragalus polysaccharide(APS) protection (group S). Group C, the drilling intracranial set the Foley ballooncatheter, but not pressurized, the other with B, S group. Group S intervention forAstragalus polysaccharide brain death group, immediately after anesthesia via thefemoral vein bolus injection of astragalus polysaccharide (APS)12mg/kg. Group Csham surgery4h (of T1), B group and S group induced brain death4h (of T1) were randomly drawn four New Zealand rabbits to take specimens, and four New Zealandrabbits in sham operation8h (the T2) and the induction of brain death after8h (T2),specimens were taken.Take blood samples to5mL from femoral artery and cut theliver tissue. Serum acute liver damage indicators alanine aminotransferase (ALT),aspartate aminotransferase (AST), enzyme-linked immunosorbent assay (ELISA) ofserum TNF-alpha. HE staining changes on liver biopsy, immunohistochemicaltechniques in liver tissues of NF-κB p65protein expression.Using the reversetranscriptase polymerase chain reaction (RT-PCR) to detecte ICAM-1mRNAtranscription level in liver tissue. Determine the superoxide dismutase (T-SOD)activity of liver tissue in T1.Results: Part I:Brain-dead group of intracranial pressure, mean arterial bloodpressure increased significantly (p<0.05); before the brain death group BD2h HR thanthe pressure decreased significantly (p<0.05); brain death group pressure after RRthan the pressure rise (p<0.05); brain death group after the cessation of rescue0.5min,3min,6min, MAP, HR was lower than the control group, the difference wasstatistically significant; stopped the rescue, B1group and the B2group heart survivaltime, with no significant difference.Part Ⅱ:(1) ALT, AST of serum, TNF-alpha level: Group C T1, T2, three indicatorsno significant difference (P>0.05). B and S-group of the same point in time weresignificantly higher than group C (P<0.05). Group B, T2indicators were significantlyhigher than T1(P<0.05). S group T2of ALT, TNF-alpha levels were significantlyhigher than T1(P<0.05) and AST two time points were no significant differences (P>0.05). S group at each time point three indicators were significantly lower than groupB (P <0.05).(2) Liver tissue NF-κB p65protein expression immunohistochemistry:Quantitative analysis of the quantitative image analysis software to measure theaverage optical density (OD) of the results of immunohistochemistry. Three groupsT1expression levels similar to the relatively weak OD values without significantdifference (P>0.05). Group B, expression of the S group at T2compared with T1significantly increased (P<0.05). C and S groups, OD values of T1, T2, no significantdifference (P>0.05). Group B expressed T2compared to T1was significantly enhanced (P<0.05). S group, the corresponding time points protein expression werelower than group B (P<0.05).(3) RT-PCR: The expression of ICAM-1mRNA transcription levels in group Cat all time points compared with no significant difference (P>0.05); B, S group at T2expression was stronger at T1(P<0.05). The expression level of the correspondingpoint in time there was significant difference (P<0.05).(4) S group in liver tissue superoxide dismutase (T-SOD) activity compared withC and Group B was significantly increased in T1(P<0.05).(5) HE staining under the light microscope: C, normal liver tissue structure.Liver cells of group B at T2was significantly increased, disorganized and crowded,the sinusoidal pressure narrowed cytoplasm loose lightly stained reticular,balloon-like changes in inflammatory cell infiltration in portal area. S group at T2liver cells increased edema, the cytoplasmic loose a small amount of inflammatoryConclusion:(1) Progressive intracranial pressure induced by brain death, through themeasures of mechanical ventilation and vasoactive drugs, a long time to maintainbrain-dead body of hemodynamic stability. After brain death, cardiac function has notdeclined with time. Stop after the rescue, MAP, HR showed a progressive decline inshort time All non-heart-beating death (Non heart beating death, NHBD).(2) brain-dead state of rabbit serum ALT and AST and TNF-α level increased.Transcriptional level in liver tissue adhesion molecules ICAM-1mRNA expressionwas elevated. The increase in NF-κB p65protein translation level in liver tissue. Theincreased degree of positive correlation with brain-dead time.(3) APS, it could safely reduce the dirty of NF-κB protein translation, mRNAexpression of ICAM-1, reduction of serum TNF-α levels and improve theorganization of oxygen free radicals SOD activity.,(4) APS brain death to cardiac death process in the rabbit liver has a protectiveeffect and its mechanism may be involved in inhibiting NF-κB by a variety of waysspecific and nonspecific inflammatory injury.